DNAdam Cancer Research Results

DNAdam, DNA damage: Click to Expand ⟱

Source: HalifaxProj(prevent)

Type:

DNA damage plays a crucial role in the development of cancer. The integrity of DNA is essential for the proper functioning of cells, and when DNA is damaged, it can lead to mutations that may contribute to cancer progression.

Scientific Papers found: Click to Expand⟱

5289-

5-HTP,

5-Hydroxytryptophan (5-HTP): Natural Occurrence, Analysis, Biosynthesis, Biotechnology, Physiology and Toxicology

Review,

AD,

Review,

Arthritis,

*5HT↑, 5-HTP plays a major role both in neurologic and metabolic diseases and its synthesis from tryptophan represents the limiting step in serotonin and melatonin biosynthesis.
*Inflam↓, 5-HTP also suppresses inflammation and arthritis through decreasing the production of pro-inflammatory mediators
*memory↑, figure 10
*Sleep↑, In a group of children with sleep terrors, treatment with 5-HTP was able to modulate the arousal level and to induce a long-term improvement of sleep terrors [1
*Weight↓, The effect of 5-HTP on feeding behavior, mood state, and weight loss was studied. 5-HTP promoted decreased food intake and weight loss as well as typical anorexia-related symptoms without changes in mood state during the period of observation
*DNAdam↓, 5-HTP significantly reduced tert-butylhydroperoxide-induced oxidative damage in human fibroblast cells and protected these cells against oxidative DNA damage
*ROS↓, By acting as a reactive oxygen species (ROS) scavenger, 5-HTP has the potential for use in the treatment of inflammatory diseases and as an analgesic
*toxicity↝, An excess of 5-HTP may be responsible for serotonin syndrome (see Section 8.2.1) and an excessive treatment was found to be associated with severe side effects, including behavioral disturbances, abnormal mental functions, and intolerance.

5352-

AL,

Anticancer potential of allicin: A review

Review,

Var,

*cardioP↑, Allicin has many health-promoting properties, such as cardioprotective, antimicrobic, cholesterol-lowering, anti-inflammatory, and antitumor.
*Bacteria↓,
*Inflam↓,
AntiTum↑,
*DNAdam↓, DNA damage protection, induction of cell death, inhibition of cell proliferation, and block of angiogenesis and metastasis formation.
TumCP↓,
angioG↓,
TumMeta↓,

3163-

Ash,

Rad,

Withaferin A, a steroidal lactone, selectively protects normal lymphocytes against ionizing radiation induced apoptosis and genotoxicity via activation of ERK/Nrf-2/HO-1 axis

*radioP↑, Withaferin A (WA) protected only normal lymphocytes, but not cancer cells, against IR-induced apoptosis
selectivity↑,
*Casp3↓, WA treatment led to significant inhibition of IR-induced caspase-3 activation and decreased IR-induced DNA damage to lymphocytes and bone-marrow cells.
*DNAdam↓,
*ROS↓, WA reduced intracellular ROS and GSH levels
*GSH↓,
*NRF2↑, WA induced pro-survival transcription factor, Nrf-2, and expression of cytoprotective genes HO-1, catalase, SOD, peroxiredoxin-2 via ERK.
*HO-1↑,
*Catalase↑,
*SOD↑,
*Prx↑,
*ERK↑, Activated ERK promotes the nuclear translocation and activity of Nrf2

4825-

ASTX,

In vivo protective efficacy of astaxanthin against ionizing radiation-induced DNA damage

in-vivo,

Nor,

4 mg/kg by gavage for 7 days starting from irradiation

Thirty-two male rats were randomly divided into four groups

*DNAdam↓, DNA damage was reduced in the radiation+astaxanthin group compared with the radiation group
*radioP↑,

5365-

AV,

Aloe Vera Polysaccharides as Therapeutic Agents: Benefits Versus Side Effects in Biomedical Applications

Review,

Nor,

Review,

IBD,

Review,

Diabetic,

*Wound Healing↑, Traditionally recognized for its anti-inflammatory and antimicrobial effects, which are very important in wound healing, the Aloe Vera relies on its polysaccharides
*Imm↑, which confer immunomodulatory, antioxidant, and tissue-regenerative properties.
*antiOx↑,
*AntiDiabetic↑, graphical abstract
*AntiCan↑,
*Inflam↓, The anti-inflammatory properties of Aloe Vera polysaccharides are primarily mediated through the inhibition of key inflammatory pathways.
*NF-kB↓, Acemannan and other polysaccharides suppress the activation of nuclear factor-kappa B (NF-κB), a transcription factor that regulates the expression of pro-inflammatory genes.
*COX2↓, By inhibiting NF-κB [48,49], Aloe Vera polysaccharides reduce the production of cyclooxygenase-2 (COX-2) and lipoxygenase (LOX),
*5LO↓,
*IL1β↓, Aloe Vera polysaccharides downregulate the expression of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, while upregulating anti-inflammatory cytokines such as IL-10
*IL6↓,
*TNF-α↓,
*IL10↑,
*other↓, This dual action helps to mitigate inflammation in conditions such as arthritis, dermatitis, and inflammatory bowel disease (IBD)
*ROS↓, Aloe Vera polysaccharides exhibit potent antioxidant activity by scavenging reactive oxygen species (ROS) and free radicals,
*SOD↑, The polysaccharides enhance the activity of endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which neutralize oxidative stress and protect cells from damage [17,63].
*Catalase↑,
*GPx↑,
*lipid-P↓, This property is particularly beneficial in preventing lipid peroxidation, DNA damage, and protein oxidation, processes associated with chronic diseases and aging
*DNAdam↓,
*GutMicro↑, Aloe Vera polysaccharides support gastrointestinal health, acting as prebiotics and promoting the growth of beneficial gut microbiota such as Lactobacillus and Bifidobacterium species [64].
*ZO-1↑, enhance the integrity of the intestinal epithelial barrier by upregulating the expression of tight junction proteins such as occludin and zonula occludens-1 (ZO-1) [51,54].
AntiTum↑, Certain polysaccharides in Aloe Vera, including acemannan, have demonstrated antitumoral effects by inducing apoptosis (programmed cell death) in cancer cells.
Casp3↑, This is achieved through the activation of caspase-3 and caspase-9, key enzymes in the apoptotic pathway [45,48].
Casp9↑,
angioG↓, Aloe Vera polysaccharides also inhibit angiogenesis and metastasis by downregulating matrix metalloproteinases (MMPs) and VEGF [75].
MMPs↓,
VEGF↓,
NK cell↑, Moreover, these polysaccharides enhance the immune system’s ability to recognize and destroy cancer cells through stimulating natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) [43,55].

2623-

Ba,

Activation of the Nrf2/HO-1 signaling pathway contributes to the protective effects of baicalein against oxidative stress-induced DNA damage and apoptosis in HEI193 Schwann cells

in-vitro,

Nor,

HEI193

50 and 100 μM

*DNAdam↓, Our results showed that baicalein effectively inhibited H2O2-induced cytotoxicity and DNA damage associated with the inhibition of reactive oxygen species (ROS) accumulation.
*ROS↓,
*Bax:Bcl2↓, increased the Bax/Bcl-2 ratio
*p‑NRF2↑, baicalein increased not only the expression but also the phosphorylation of nuclear factor-erythroid 2 related factor 2 (Nrf2) and promoted the expression of heme oxygenase-1 (HO-1)
*HO-1↑, it is well known that the antioxidant efficacy of baicalein is related to the activation of the Nrf2/HO-1 signaling pathway
*neuroP↑, suggested that baicalein may have a beneficial effect on the prevention and treatment of peripheral neuropathy induced by oxidative stress.
*MMP↑, inhibitory effect of baicalein on MMP reduction

2689-

BBR,

Berberine protects against glutamate-induced oxidative stress and apoptosis in PC12 and N2a cells

in-vitro,

Nor,

PC12

in-vitro,

AD,

in-vitro,

Stroke,

*ROS↓, In both cell lines, pretreatment with berberine (especially at low concentrations) significantly decreased ROS generation, lipid peroxidation, and DNA fragmentation, while improving glutathione content and SOD activity in glutamate-injured cells.
*lipid-P↓,
*DNAdam↓, Berberine significantly diminished glutamate-induced DNA fragmentation
*GSH↑,
*SOD↑,
*eff↑, This is relevant to berberine treatment in neurodegenerative disorders, such as dementia (Alzheimer’s disease), seizures, and stroke.
*cl‑Casp3↓, Berberine significantly decreased cleaved caspase-3 and bax/bcl-2 expressions in the glutamate-injured cells
*BAX↓,
*neuroP↑, the current study demonstrated that berberine exerts neuroprotective effects against glutamate-induced N2a and PC12 cytotoxicity via antioxidant and anti-apoptotic mechanisms
*Dose↝, the protective effect of berberine was more significant at lower concentrations and decreased with increasing concentration.
*Ca+2↓, Nadjafi et al demonstrated that berberine protects OLN-93 oligodendrocytes against ischemic-induced cell death by attenuating the intracellular Ca2+ overload similar to the NMDA or the AMPA/kainate receptors antagonists

3514-

Bor,

CUR,

Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta

in-vivo,

AD,

rat

*DNAdam↓, Co-administration of BA and curcumin on synaptosomes exposed to Aβ1-42 resulted in a significant decrease in DNA fragmentation values, MDA levels, and AChE activities.
*MDA↓,
*AChE↓,
*neuroP↑, BA and curcumin had protective effects on rat brain synaptosomes against Aβ1-42 exposure.
*ROS↓, BA and curcumin treatment can have abilities to prevent the alterations of the cholinergic system and inhibit oxidative stress in the cerebral cortex synapses of Aβ1-42 exposed.
*NO↓, Synaptosomes treated with BA showed a significant reduction in MDA and NO levels

4272-

Bor,

Neuroprotective properties of borax against aluminum hydroxide-induced neurotoxicity: Possible role of Nrf-2/BDNF/AChE pathways in fish brain

*NRF2↑, BX clearly activating the Nrf-2/ROS signaling pathway.
*ROS↓,
*antiOx↑, BX supported antioxidant capacity without leading apoptosis, lipid peroxidation, inflammatory response and DNA damage.
*lipid-P↑,
*Inflam↓,
*DNAdam↓,
*BDNF↑, BX also increased the BDNF levels and AChE activity.
*neuroP↑, BX exerted a neuroprotective effect against AH-induced neurotoxicity via down-regulating cytokine-related pathways, minimising DNA damage, apoptosis
*GSH↑, as well as up-regulating GSH, AChE, BDNF and antioxidant enzyme levels.

1425-

Bos,

Protective Effect of Boswellic Acids against Doxorubicin-Induced Hepatotoxicity: Impact on Nrf2/HO-1 Defense Pathway

in-vivo,

Nor,

*ChemoSen↑, BAs significantly improved the altered liver enzyme activities and oxidative stress markers.
*NRF2↑, BAs increased the Nrf2 and HO-1 expression, which provided protection against DOX-induced oxidative insult
*HO-1↑,
*ROS↓, appear to scavenge ROS and inhibit lipid peroxidation and DNA damage of DOX-induced hepatotoxicity
*lipid-P↓,
*DNAdam↓,

5916-

Cats,

Chemo,

Uncaria tomentosa—Adjuvant Treatment for Breast Cancer: Clinical Trial

Trial,

BC,

UtCa received chemotherapy plus 300 mg dry Ut extract per day and the Ca group that only received chemotherapy

*DNAdam↓, Uncaria tomentosa reduced the neutropenia caused by chemotherapy and was also able to restore cellular DNA damage.
Neut↓, A greater reduction in the white blood cell (WBCs) and the neutrophil counts were observed in the Ca group along the treatment, differently from the UtCa group, which remained closely the reference values
eff↑, We concluded that Ut is an effective adjuvant treatment for breast cancer.
Imm↑, Uncaria tomentosa enables the stimulation of the immune system, increasing resistance to diseases
Dose↝, Treatment using a daily dose of 300 mg dry Ut extract was effective in reducing the main chemotherapy effect, which is neutropenia.

3997-

CoQ10,

Coenzyme Q and Its Role in the Dietary Therapy against Aging

Review,

AD,

*AntiAge↑, anti-aging potential of CoQ and its possible use in dietary therapies to alleviate the effects of aging.
*Inflam↓, CoQ Exerts Anti-Inflammatory Effects through Its Antioxidant Activity
*antiOx↑,
*Apoptosis↓, protective role of CoQ10 against apoptosis by inducing the inhibition of cell death independently from its free radical scavenging properties or antioxidant effects
*BioAv↑, It has been reported that intestinal absorption is threefold faster if CoQ10 is administrated with food intake in rats
*other↝, Actually, it has been reported that NQO1 expression increases during the initial steps of Alzheimer’s disease, indicating a higher lipid peroxidation coupled to a higher necessity for CoQ-dependent antioxidant activity
*cognitive↑, In older mice with clear cognitive and psychomotor impairments, short-time (15 days) CoQ-supplementation improved spatial learning
*DNAdam↓, dietary CoQ has also been shown to improve DNA repair systems [213,214] and modulate inflammatory signaling cascade as well as to reduce endoplasmic reticulum stress [214].
*ER Stress↓,

5801-

CRMs,

Chemo,

Caloric Restriction Enhances Chemotherapy Efficacy and Reshapes Stress Responses in Sarcoma

in-vivo,

sarcoma,

Mice bearing Sarcoma-180

TumCG↓, It was found that this combined approach reduced tumor growth more effectively than chemotherapy alone and helped protect the blood, liver, and DNA from treatment-related damage.
*hepatoP↑,
*ROS↓, It also lowered oxidative stress and improved survival.
*OS↑, Caloric Restriction Combined with Chemotherapy Revealed Increased Survival in Sarcoma-Bearing Animals. Caloric restriction improved survival by approximately 81.82% compared to standard treatment
ChemoSen↑, promising approach to enhance the effects of chemotherapy and mitigate its adverse effects.
chemoPv↑,
selectivity↑, Together, these results indicate that caloric restriction enhances the antitumor effect of doxorubicin while offering protection to healthy tissues.
*DNAdam↓, Caloric restriction combined with chemotherapy (CRDOX) reduced DNA damage in peripheral blood cells.

1605-

EA,

Ellagic Acid and Cancer Hallmarks: Insights from Experimental Evidence

Review,

Var,

*BioAv↓, Within the gastrointestinal tract, EA has restricted bioavailability, primarily due to its hydrophobic nature and very low water solubility.
antiOx↓, strong antioxidant properties [12,13], anti-inflammatory effects
Inflam↓,
TumCP↓, numerous studies indicate that EA possesses properties that can inhibit cell proliferation
TumCCA↑, achieved this by causing cell cycle arrest at the G1 phase
cycD1/CCND1↓, reduction of cyclin D1 and E levels, as well as to the upregulation of p53 and p21 proteins
cycE/CCNE↓,
P53↑,
P21↑,
COX2↓, notable reduction in the protein expression of COX-2 and NF-κB as a result of this treatment
NF-kB↓,
Akt↑, suppressing Akt and Notch signaling pathways
NOTCH↓,
CDK2↓,
CDK6↓,
JAK↓, suppression of the JAK/STAT3 pathway
STAT3↓,
EGFR↓, decreased expression of epidermal growth factor receptor (EGFR)
p‑ERK↓, downregulated the expression of phosphorylated ERK1/2, AKT, and STAT3
p‑Akt↓,
p‑STAT3↓,
TGF-β↓, downregulation of the TGF-β/Smad3
SMAD3↓,
CDK6↓, EA demonstrated the capacity to bind to CDK6 and effectively inhibit its activity
Wnt/(β-catenin)↓, ability of EA to inhibit phosphorylation of EGFR
Myc↓, Myc, cyclin D1, and survivin, exhibited decreased levels
survivin↓,
CDK8↓, diminished CDK8 level
PKCδ↓, EA has demonstrated a notable downregulatory impact on the expression of classical isoenzymes of the PKC family (PKCα, PKCβ, and PKCγ).
tumCV↓, EA decreased cell viability
RadioS↑, further intensified when EA was combined with gamma irradiation.
eff↑, EA additionally potentiated the impact of quercetin in promoting the phosphorylation of p53 at Ser 15 and increasing p21 protein levels in the human leukemia cell line (MOLT-4)
MDM2↓, finding points to the ability of reduced MDM2 levels
XIAP↓, downregulation of X-linked inhibitor of apoptosis protein (XIAP).
p‑RB1↓, EA exerted a decrease in phosphorylation of pRB
PTEN↑, EA enhances the protein phosphatase activity of PTEN in melanoma cells (B16F10)
p‑FAK↓, reduced phosphorylation of focal adhesion kinase (FAK)
Bax:Bcl2↑, EA significantly increases the Bax/Bcl-2 rati
Bcl-xL↓, downregulates Bcl-xL and Mcl-1
Mcl-1↓,
PUMA↑, EA also increases the expression of Bcl-2 inhibitory proapoptotic proteins PUMA and Noxa in prostate cancer cells
NOXA↑,
MMP↓, addition to the reduction in MMP, the release of cytochrome c into the cytosol occurs in pancreatic cancer cells
Cyt‑c↑,
ROS↑, induction of ROS production
Ca+2↝, changes in intracellular calcium concentration, leading to increased levels of EndoG, Smac/DIABLO, AIF, cytochrome c, and APAF1 in the cytosol
Endoglin↑,
Diablo↑,
AIF↑,
iNOS↓, decreased expression of Bcl-2, NF-кB, and iNOS were observed after exposure to EA at concentrations of 15 and 30 µg/mL
Casp9↑, increase in caspase 9 activity in EA-treated pancreatic cancer cells PANC-1
Casp3↑, EA-induced caspase 3 activation and PARP cleavage in a dose-dependent manner (10–100 µmol/L)
cl‑PARP↑,
RadioS↑, EA sensitizes and reduces the resistance of breast cancer MCF-7 cells to apoptosis induced by γ-radiation
Hif1a↓, EA reduced the expression of HIF-1α
HO-1↓, EA significantly reduced the levels of two isoforms of this enzyme, HO-1, and HO-2, and increased the levels of sEH (Soluble epoxide hydrolase) in LnCap
HO-2↓,
SIRT1↓, EA-induced apoptosis was associated with reduced expression of HuR and Sirt1
selectivity↑, A significant advantage of EA as a potential chemopreventive, anti-tumor, or adjuvant therapeutic agent in cancer treatment is its relative selectivity
Dose∅, EA significantly reduced the viability of cancer cells at a concentration of 10 µmol/L, while in healthy cells, this effect was observed only at a concentration of 200 µmol/L
NHE1↓, EA had the capacity to regulate cytosolic pH by downregulating the expression of the Na+/H+ exchanger (NHE1)
Glycolysis↓, led to intracellular acidification with subsequent impairment of glycolysis
GlucoseCon↓, associated with a decrease in the cellular uptake of glucose
lactateProd↓, notable reduction in lactate levels in supernatant
PDK1?, inhibit pyruvate dehydrogenase kinase (PDK) -bind and inhibit PDK3
PDK1?,
ECAR↝, EA has been shown to influence extracellular acidosis
COX1↓, downregulation of cancer-related genes, including COX1, COX2, snail, twist1, and c-Myc.
Snail↓,
Twist↓,
cMyc↓,
Telomerase↓, EA, might dose-dependently inhibit telomerase activity
angioG↓, EA may inhibit angiogenesis
MMP2↓, EA demonstrated a notable reduction in the secretion of matrix metalloproteinase (MMP)-2 and MMP-9.
MMP9↓,
VEGF↓, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
Dose↝, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
PD-L1↓, EA downregulated the expression of the immune checkpoint PD-L1 in tumor cells
eff↑, EA might potentially enhance the efficacy of anti-PD-L1 treatment
SIRT6↑, EA exhibited statistically significant upregulation of sirtuin 6 at the protein level in Caco2 cells
DNAdam↓, increase in DNA damage

2846-

FIS,

Fisetin protects against cardiac cell death through reduction of ROS production and caspases activity

in-vitro,

Nor,

0, 5, 10, 15, 20, 30, 40, 60, 80 and 100 μM

concentration of 15 μM of fisetin in the subsequent experiments

*cardioP↑, Fisetin enhances viability of rat cardiomyocytes following hypoxia/starvation – reoxygenation.
*ROS↓, It inhibits apoptosis, decreases ROS generation and caspase activation and protects from DNA damage
*Casp↓,
*DNAdam↓,

4511-

GLA,

Gamma-Linolenic Acid (GLA) Protects against Ionizing Radiation-Induced Damage: An In Vitro and In Vivo Study

vitro+vivo,

Nor,

RAW264.7

*radioP↑, mice exposed to lethal radiation (survival~20%) is significantly enhanced (to ~80%) by GLA treatment
*ROS↓, GLA reduced DNA damage (as evidenced by micronuclei formation) and enhanced metabolic viability, which led to an increase in the number of surviving RAW 264.7 cells in vitro by reducing ROS generation
*DNAdam↓, GLA reduced DNA damage
*IL6↓, by restoring altered levels of duodenal HMGB1, IL-6, TNF-α, and IL-10 concentrations, as well as the expression of NF-kB, IkB, Bcl-2, Bax, delta-6-desaturase, COX-2, and 5-LOX genes, and pro- and anti-oxidant enzymes (SOD, catalase, glutathione), to
*TNF-α↓,
*IL10↓,
*NF-kB↓,
*SOD↑, GLA pre-treated RAW cells (GLA + irradiation) showed improved antioxidant status and a significant (p < 0.01) increase in SOD, catalase, and GPx
*Catalase↑,
*GSH↑,

1787-

LE,

Licorice and cancer

Review,

Var,

Inflam↓, known or suspected (anti-inflammatory, antivirus, antiulcer, anticarcinogenesis, and others
AntiCan↓,
DNAdam↓, Licorice and its derivatives may protect against carcinogen-induced DNA damage
LOX1↓, Glycyrrhizic acid is an inhibitor of lipoxygenase and cyclooxygenase, inhibits protein kinase C, and downregulates the epidermal growth factor receptor
COX2↓,
PKCδ↓,
EGFR↓,

3268-

Lyco,

Lycopene as a Natural Antioxidant Used to Prevent Human Health Disorders

Review,

AD,

*BioAv↓, Lycopene bioavailability can be decreased by ageing, and some of the pathological states, such as cardiovascular diseases (CVDs)
*AntiCan↑, For instance, it has been shown that a higher dietary intake and circulating concentration of lycopene have protective effects against prostate cancer (PCa), in a dose-dependent way
*ROCK1↓, It remarkably lessened the expression of ROCK1, Ki-67, ICAM-1 and ROCK2,
*Ki-67↓,
*ICAM-1↓,
*cardioP↑, Lycopene is a cardioprotective nutraceutical.
*antiOx↑, Lycopene is a well-known antioxidant.
*NQO1↑, Furthermore, lycopene supplementation improves mRNA expressions of the NQO-1 and HO-1 as antioxidant enzymes.
*HO-1↑,
*TNF-α↓, downregulate inflammatory cytokines (i.e., TNF-α, and IL-1β) in the hippocampus of the mice.
*IL22↓,
*NRF2↑, Lycopene decreased neuronal oxidative damage by activating Nrf2, as well as by inactivating NF-κB translocation in H2O2-related SH-SY5Y cell model
*NF-kB↓,
*MDA↓, significantly reduced the malondialdehyde (MDA)
*Catalase↑, Furthermore, it improved the catalase (CAT), superoxide dismutase (SOD), and GSH levels, and antioxidant capacity [109].
*SOD↑,
*GSH↑,
*cognitive↑, Lycopene administration considerably improved cognitive defects, noticeably reduced MDA levels and elevated GSH-Px activity, and remarkably reduced tau
*tau↓,
*hepatoP↑, Lycopene was also found to be effective against hepatotoxicity by acting as an antioxidant, regulating total glutathione (tGSH) and CAT concentrations
*MMP2↑, It also elevated MMP-2 down-regulation
*AST↓, lowering the liver enzymes levels, like aspartate transaminase (AST), alanine transaminase (ALT), LDL, free fatty acid, and MDA.
*ALAT↓,
*P450↑, Moreover, tomato powder has been shown to have a protective agent against alcohol-induced hepatic injury by inducing cytochrome p450 2E1
*DNAdam↓, lycopene decreased DNA damage
*ROS↓, It has been revealed that they inhibited ROS production, protected antioxidant enzymes, and reversed hepatotoxicity in rats’ liver
*neuroP↑, lycopene consumption relieved cognitive defects, age-related memory loss, neuronal damage, and synaptic dysfunction of the brain.
*memory↑,
*Ca+2↓, Lycopene suppressed the 4-AP-invoked release of glutamate and elevated intra-synaptosomal Ca2+ level.
*Dose↝, an in vivo study revealed that lycopene (6.5 mg/day) was effective against cancer in men [147]. However, lycopene dose should be increased up to 10 mg/day, in the case of advanced PCa.
*Dose↑, lycopene supplementation (15 mg/day, for 12 weeks) in an old aged population improved immune function through increasing natural killer cell activity by 28%
*Dose↝, Finally, according to different epidemiological studies, daily lycopene intake can be suggested to be 2 to 20 mg per day
*toxicity∅, A toxicological study on rats showed the no-observed-adverse-effect level at the highest examined dose (i.e., 1.0% in the diet)
PGE2↓, Lycopene doses of 0, 10, 20, and 30 µM were used to treat human colorectal cancer cell. Prostaglandin E2 (PGE2), and NO levels declined after lycopene administration,
CDK2↓, Treatment with lycopene reduced cell hyperproliferation induced by UVB and ultimately promoted apoptosis and reduced CDK2 and CDK4 complex in SKH-1 hairless mice
CDK4↓,
STAT3↓, lycopene reduced the STAT3 expression in ovarian tissues
NOX↓, (SK-Hep-1) cells and indicated a substantial reduction in NOX activity. Moreover, it inhibits the protein expression of NOX4, NOX4 mRNA and ROS intracellular amounts
NOX4↓,
ROS↓,
*SREBP1↓, Lycopene decreases the fatty acid synthase (FAS), sterol regulatory element-binding protein 1c (SREBP-1c), and Acetyl-CoA carboxylase (ACC1) expression in HFD mice.
*FASN↓,
*ACC↓,

3277-

Lyco,

Recent trends and advances in the epidemiology, synergism, and delivery system of lycopene as an anti-cancer agent

Review,

Var,

antiOx↑, lycopene provides a strong antioxidant activity that is 100 times more effective than α-tocopherol and more than double effective that of β-carotene
TumCP↓, In vivo and in vitro experiments have demonstrated that lycopene at near physiological levels (0.5−2 μM) could inhibit cancer cell proliferation [[22], [23], [24]], induce apoptosis [[25], [26], [27]], and suppress metastasis [
Apoptosis↑,
TumMeta↑,
ChemoSen↑, lycopene can increase the effect of anti-cancer drugs (including adriamycin, cisplatin, docetaxel and paclitaxel) on cancer cell growth and reduce tumour size
BioAv↓, low water solubility and bioavailability of lycopene
Dose↝, The concentration of lycopene in plasma (daily intake of 10 mg lycopene) is approximately 0.52−0.6 μM
BioAv↓, significant decrease in lycopene bioavailability in the elderly
BioAv↑, oils and fats favours the bioavailability of lycopene [80], while large molecules such as pectin can hinder the absorption of lycopene in the small intestine due to their action on lipids and bile salt molecules
SOD↑, GC: 50−150 mg/kg BW/day ↑SOD, CAT, GPx ↑IL-2, IL-4, IL-10, TNF-α ↑IgA, IgG, IgM ↓IL-6
Catalase↑,
GPx↑,
IL2↑, lycopene treatment significantly enhanced blood IL-2, IL-4, IL-10, TNF-α levels and reduced IL-6 level in a dose-dependent manner.
IL4↑,
IL1↑,
TNF-α↑,
GSH↑, GC: ↑GSH, GPx, GST, GR
GPx↑,
GSTA1↑,
GSR↑,
PPARγ↑, ↑GPx, SOD, MDA ↑PPARγ, caspase-3 ↓NF-κB, COX-2
Casp3↑,
NF-kB↓,
COX2↓,
Bcl-2↑, AGS cells Lycopene 5 μM ↑Bcl-2 ↓Bax, Bax/Bcl-2, p53 ↓Chk1, Chk2, γ-H2AX, DNA damage ↓ROS Phase arrest
BAX↓,
P53↓,
CHK1↓,
Chk2↓,
γH2AX↓,
DNAdam↓,
ROS↓,
P21↑, CRC: ↑p21 ↓PCNA, β-catenin ↓COX-2, PGE2, ERK1/2 phosphorylated
PCNA↓,
β-catenin/ZEB1↓,
PGE2↓,
ERK↓,
cMyc↓, AGS cells: ↓Wnt-1, c-Myc, cyclin E ↓Jak1/Stat3, Wnt/β-catenin alteration ↓ROS
cycE/CCNE↓,
JAK1↓,
STAT3↓,
SIRT1↑, Huh7: ↑SIRT1 ↓Cells growth ↑PARP cleavage ↓Cyclin D1, TNFα, IL-6, NF-κB, p65, STAT3, Akt activation ↓Tumour multiplicity, volume
cl‑PARP↑,
cycD1/CCND1↓,
TNF-α↓,
IL6↓,
p65↓,
MMP2↓, SK-Hep1 human hepatoma cells Lycopene 5, 10 μM ↓MMP-2, MMP-9 ↓
MMP9↓,
Wnt↓, AGS cells Lycopene 0.5 μM, 1 μM ↓Wnt-1, c-Myc, cyclin E ↓Jak1/Stat3, Wnt/β-catenin alteration ↓ROS

4780-

Lyco,

Potential inhibitory effect of lycopene on prostate cancer

Review,

Pca,

TumCP↓, Lycopene suppress the progression and proliferation
TumCCA↑, Lycopene has been found to effectively suppress the progression and proliferation, arrest in-cell cycle, and induce apoptosis of prostate cancer cells in both in-vivo and in-vitro conditions.
Apoptosis↑,
*neuroP↑, the neuro-protective effect of lycopene, mediates the signaling pathways, by inhibiting NF-κB (nuclear factor-κB) and JNK protein (c-Jun N-terminal kinase), and activating Nrf2 (Nuclear factor erythroid 2-related factor 2) and BDNF (
*NF-kB↓,
*JNK↓,
*NRF2↑,
*BDNF↑,
*Ca+2↝, as well as keeping homeostasis by restoring intracellular Ca2+
*antiOx↑, most powerful and natural antioxidants, and its role in preventing prostate cancer.
*AntiCan↑,
*Inflam↓, Anti-inflammatory properties of lycopene depends on time, and it has been found to be through the decrease of inflammatory cytokines (i.e. IL1, IL6, IL8 and tumor necrosis factor-α (TNF-α)
*IL1↓,
*IL6↓,
*IL8↓,
*TNF-α↓,
NF-kB↓, lycopene increased the expression of BCO2 enzyme in an androgen-sensitive cell line that prevented cancer cell proliferation and reduced the NF-κB activity
DNAdam↓, 20 and 50 μM doses of lycopene had an effect on PC3 and DU145 cell lines in inducing apoptosis with DNA damages, and preventing cell growth and colony formation
PSA↓, lycopene twice a day for 3 weeks, showed that lycopene decreases the risk and growth of prostate cancer cells, and also a decrease in the level of PSA,
P53↓, down-regulation of p53, Cyclin-D1, and Nrf-2 have occurred after the incubation of prostate cancer cells with the lycopene received patient’s sera in comparison with placebo
cycD1/CCND1↓,
NRF2↓,
Akt2↓, treatment with lycopene in PC3 cancer cell lines was associated with down-regulation of AKT2 [
PPARγ↓, Another anti-proliferative effect of lycopene was done by increasing PPARγ-LXRα-ABCA1signaling molecules in protein and mRNA level

4794-

Lyco,

Anticancer Effect of Lycopene in Gastric Carcinogenesis

Review,

GC,

*AntiCan↑, Lycopene from red fruits and vegetables has strong anticancer activity in gastric carcinogenesis.
*ROS↓, As one of the most potent antioxidants, lycopene is effective in decreasing oxidative damage by activating antioxidant enzymes such as GSH, GPx and GST.
*GSH↑,
*GPx↑,
*GSTs↑,
TumCG↓, Lycopene treatment inhibits cancer cell growth and induces apoptosis by suppressing ERK signaling pathway.
Apoptosis↑,
ERK↓,
Bcl-2↓, Lycopene decreases Bcl-2 and increases Bax expression, which induce release of cytochrome C from mitochondria, leading to apoptosis.
BAX↑,
Cyt‑c↑,
TumCCA↑, Lycopene treatment inhibits gastric cancer cell proliferation by increasing cell cycle arrest in G0–G1 phase
*DNAdam↓, Lycopene inhibits H. pylori-induced increases in ROS levels and DNA damage in gastric epithelial cells

3844-

Moringa,

Review of the Safety and Efficacy of Moringa oleifera

Review,

NA,

*antiOx↑, biological activities including antioxidant, tissue protective (liver, kidneys, heart, testes, and lungs), analgesic, antiulcer, antihypertensive, radioprotective, and immunomodulatory actions.
*RenoP↑,
*hepatoP↑,
*radioP↑, Two studies have shown that extracts of M. oleifera can provide radioprotection in mice.
*eff↑, leaves are widely used as a basic food because of their high nutrition content
*toxicity↓, authors concluded that consumption of M. oleifera leaves at doses of up to 2000 mg/kg were safe.
*ROS↓, Chumark et al. (2008) demonstrated the free radical scavenging ability of an aqueous extract of M. oleifera leaves in several in vitro systems, and also showed that the extract inhibited lipid peroxidation in both in vitro and ex vivo systems.
*lipid-P↓,
*DNAdam↓, inhibit oxidative damage to DNA
*Catalase↑, increased the antioxidant enzymes catalase and superoxide dismutase while decreasing lipid peroxidases
*SOD↑,
*GPx↑, increases in the antioxidant enzymes glutathione peroxidase, glutathione reductase, catalase, superoxide dismutase, and glutathione S‐transferase (Sreelatha and Padma, 2010).
*GSR↑,
*GSTs↑,
*AST↓, M. oleifera leaves protects against liver damage as demonstrated by reductions in tissue histopathology and serum activities of marker enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP)
*ALAT↓,
*ALP↓,
*Bil↓, extract decreased drug‐induced levels of AST, ALT, ALP, and bilirubin

4035-

NAD,

VitB3,

NAD+ supplementation reduces neuroinflammation and cell senescence in a transgenic mouse model of Alzheimer's disease via cGAS-STING

in-vitro,

AD,

mouse

*Inflam↓, Treatment of AD mice with NR reduced neuroinflammation, attenuated DNA damage, and prevented cellular senescence.
*DNAdam↓,
*NLRP3↓, NR treatment also reduced NLRP3 inflammasome expression, DNA damage, apoptosis, and cellular senescence in the AD mouse brains.
*cGAS–STING↓, cGAS–STING elevation was observed in the AD mice and normalized by NR treatment

4036-

NAD,

VitB3,

NAD+ supplementation normalizes key Alzheimer’s features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency

in-vivo,

AD,

mouse

*Inflam↓, NAD+ supplementation with nicotinamide riboside significantly normalized neuroinflammation, synaptic transmission, phosphorylated Tau, and DNA damage as well as improved learning and memory and motor function.
*p‑tau↓, NR Decreases Tau Phosphorylation but Not Aβ Accumulation in AD and AD/Polβ Mice.
*DNAdam↓,
*memory↑,
*motorD↑,
*cognitive↑, NR improved cognitive function in multiple behavioral tests and restored hippocampal synaptic plasticity in 3xTgAD mice and 3xTgAD/Polβ+/− mice.
*BBB↑, NR enters the brain and boosts cellular NAD+ levels when administered orally.
IL1β↓, AD/Polβ mice had elevated levels of proinflammatory cytokines and chemokines, including IL-1α, TNFα, MCP-1, IL-1β, MIP-1α, and RANTES, and decreased levels of antiinflammatory cytokines such as IL-10 (Fig. 3G and Fig. S4A). NR treatment normalized
*TNF-α↓,
*MCP1↓,
*RANTES↓,
*ROS↓, NR treatment of AD fibroblasts resulted in decreased levels of mitochondrial ROS compared with vehicle-treated cells
*SIRT3↑, NR Treatment Decreases DNA Damage and Apoptosis Through SIRT3 and SIRT6.
*SIRT6↑,

2933-

NAD,

Nicotinamide mononucleotide (NMN) as an anti-aging health product – Promises and safety concerns

Review,

Nor,

NA,

AD,

NA,

Diabetic,

NA,

Stroke,

NA,

LiverDam,

NA,

Park,

*mtDam↓, The mitochondrial decay, which is responsible for aging, can be reversed by the increased levels of nicotinamide adenine dinucleotide (NAD+) in the body.
*BioAv↝, NMN is a precursor of NAD+ that acts as an intermediate in NAD+ biosynthesis, while dietary supplements of NMN are found to increase the NAD+ levels in the body
*BioAv↑, molecular weight is 334.22 g/mol. It is fairly acidic and water-soluble compound. The solubility has been reported to be 1.8 mg/mL
*OS↑, plays a vital role in a variety of biological processes of the body including cell death, aging, gene expression, neuroinflammation and DNA repair, which indicating a significance role of NAD+ in longevity and health of human life
*eff↑, NMN has therapeutic effects towards a range of diseases, including age-induced type 2 diabetes, obesity, cerebral and cardiac ischemia, heart failure and cardiomyopathies
*eff↑, Alzheimer’s disease and other neurodegenerative disorders, corneal injury, macular degeneration and retinal degeneration, acute kidney injury and alcoholic liver disease
*cognitive↑, cognitive impairments, DNA damage and sirtulin gene inactivation, are brought about by aging which can be evaded by enhancing NAD+ count in the body
*DNAdam↓,
*SIRT1↑, NMN, the NAMPT reaction product, is able to be utilised to trigger the SIRT1 activity
*cardioP↑, NMN also can restore gene expression linked to circadian rhythm, inflammatory response and oxidative stress, and improve hepatic insulin sensitivity, partially by SIRT1 activation.
*ROS↓, NMN has been proven to reduce DNA damage and accumulation of ROS
*Dose↝, NMN in available commercial products vary from 50 to 150 mg/capsule, whereas some consumers take two 150 mg capsules per day
*BioAv↑, NMN was speedily absorbed in the small intestine by a specific transporter, which was encoded by the Slc12a8 gene as demonstrated in in vitro and in vivo studies
*hepatoP↑, NMN supplementation has been found to have significant recovering effects on hepatocyte functions and liver pathologies in early-stage of ethanol toxicity, instead of causing adverse effects to the liver
*eff↑, supplementation of NMN has been found to be a promising therapeutic remedy for PD
*BG↓, Oral administration of NMN increased serum bilirubin contents and decreased blood glucose, chloride and serum creatinine levels, but within the normal range.
*creat↓,

2936-

NAD,

The Safety and Antiaging Effects of Nicotinamide Mononucleotide in Human Clinical Trials: an Update

*ROS↓, vitro/in vivo studies have demonstrated that NMN supplementation increases NAD+ concentration and could mitigate aging-related disorders such as oxidative stress, DNA damage, neurodegeneration, and inflammatory responses.
*DNAdam↓,
*neuroP↑, NAD+ concentrations in the human brain declined 10% to 25% from young adulthood to old age
*Inflam↓,
*BioAv↑, In fact, it has been shown that caloric restriction increases NAD+ bioavailability by activating
*SIRT1↑, whereas it lowers NADH levels and activates sirtuins to extend the life span of yeast
BioAv↝, NR holds an edge over NMN because cells cannot directly absorb NMN, and NMN must be converted to NR before entering cells.

2939-

NAD,

Rad,

NMN ameliorated radiation induced damage in NRF2-deficient cell and mice via regulating SIRT6 and SIRT7

in-vitro,

Nor,

*SIRT6↑, NMN, the agonist of SIRT6/7, alleviated DNA damage in NRF2 KO cells.
*DNAdam↓,
*radioP↑, Administration of NMN could reverse IR induced intestinal injury in NRF2−/− mice.
*ROS↓, concomitant with reduced cellular ROS level and ameliorated DNA damage

1680-

PBG,

Protection against Ultraviolet A-Induced Skin Apoptosis and Carcinogenesis through the Oxidative Stress Reduction Effects of N-(4-bromophenethyl) Caffeamide, a Propolis Derivative

in-vitro,

Nor,

HS68

*ROS↓, K36H reduced UVA-induced intracellular reactive oxygen species generation
*NRF2↑, increased nuclear factor erythroid 2–related factor 2 translocation into the nucleus to upregulate the expression of heme oxygenase-1, an intrinsic antioxidant enzyme.
*HO-1↑,
*cJun↓, K36H inhibited UVA-induced activation of extracellular-signal-regulated kinases and c-Jun N-terminal kinases,
*MMP1↓, reduced the overexpression of matrix metalloproteinase (MMP)-1 and MMP-2
*MMP2↓,
*p‑cJun↓, K36H inhibited the phosphorylation of c-Jun and downregulated c-Fos expression
*cFos↓,
*BAX↓, K36H attenuated UVA-induced Bax and caspase-3 expression and upregulated antiapoptotic protein B-cell lymphoma 2 expression.
*Casp3↓,
*DNAdam↓, K36H reduced UVA-induced DNA damage.
*iNOS↓, K36H also downregulated inducible nitric oxide synthase, cyclooxygenase-2 and interleukin-6 expression as well as the subsequent generation of prostaglandin E2 and nitric oxide.
*COX2↓,
*IL6↓,
*PGE2↓,
*NO↓,

3053-

RES,

Resveratrol represses estrogen-induced mammary carcinogenesis through NRF2-UGT1A8-estrogen metabolic axis activation

in-vitro,

NA,

MCF-10A cells were transfected with siRNA of NRF2 (siNRF2) virus plasmid

NRF2↑, whereas treatment with resveratrol could upregulate the expression of NRF2 and UGT1A8, accelerate metabolic elimination of catechol estrogens, inhibit estrogen-induced DNA damage and suppress the pathological development of breast cancer.
DNAdam↓, esveratrol attenuates mammary carcinogenesis through inhibiting estrogen-induced DNA damage

4492-

Se,

Selenium in cancer prevention: a review of the evidence and mechanism of action

Review,

Var,

Risk↓, Since as early as the 1960s geographical studies have shown a consistent trend for populations with low Se intakes to have higher cancer mortality rates
AntiCan↑, Interventions with Sehave shown benefit in reducing the risk of cancer incidence and mortality in all cancers combined, and specifically in liver, prostate, colo-rectal and lung cancers.
*selenoP↑, data showing an effect of selenoprotein genotype on cancer risk implies that selenoproteins are indeed implicated
TumMeta↓, There is some evidence that Se may affect not only cancer risk but also progression and metastasis.
*DNAdam↓, Supplementation of the diet of sexually-intact elderly male dogs with Se, as selenomethionine or high-Se yeast, at 3 or 6 ug/kg body weight per d for 7 months was found to reduce DNA damage and up-regulate epithelial cell apoptosis in their prostate
OS↑, significant secondary end-point effects of 50% lower total cancer mortality and 37% lower total cancer incidence were found, with fewer prostate, colo–rectal and lung cancers(200 ug Se (as Se-enriched yeast)/d
*ROS↓, ability of Se in selenoproteins to reduce oxidative stress is relevant to its anti-cancer effects.

4613-

Se,

Rad,

Effect of Selenium and Selenoproteins on Radiation Resistance

Review,

Nor,

*selenoP↑, GPX1 is a selenoprotein with an active site containing selenocysteine
*GPx1↑,
*GPx4↑, GPX4 effectively inhibits lipid peroxide, it also promotes DNA repair
*lipid-P↓,
*DNAdam↓,
*ROS↓, It has been reported that selenium and selenoproteins can scavenge ROS directly.
*radioP↑, selenium and selenium protein as radiation protective agents to alleviate multiple organ damage caused by radiation or treat related diseases.

4715-

Se,

The Interaction of Selenium with Chemotherapy and Radiation on Normal and Malignant Human Mononuclear Blood Cells

chemoP↑, Selenium, a trace element with anticancer properties, can reduce harmful toxicities of chemotherapy and radiotherapy without compromising efficacy.
radioP↑,
selectivity↑, MSA, at lower concentrations, induced protective responses in normal cells but cytotoxic effects in malignant cells, alone and in conjunction with chemotherapy or radiation.
ChemoSen↑, potentially improve efficacy of anticancer treatments.
GSH↓, Furthermore, the depletion of GSH by MSA in malignant THP1 cells was still significantly reduced at 24 h after radiation and chemotherapy treatment, again without the advantage of higher MSA concentrations
*GSH↑, The GSH increase in normal PBMCs was maintained at 24 h when cells were also treated with 2 Gy radiation, cytosine arabinoside (AraC) or doxorubicin (Dox), though the maximum benefit was achieved with 2.5 µM MSA
*DNAdam↓, MSA Reduces DNA Damage in Normal Cells While Increasing DNA Damage in Malignant Cells
DNAdam↑,
eff↑, The simultaneous increase in GSH in normal cells and depletion of GSH in malignant cells may contribute to improving the therapeutic ratio of cancer treatment by reducing normal tissue toxicities while increasing the anticancer efficacy.

4612-

SeNPs,

Rad,

Histopathological Evaluation of Radioprotective Effects: Selenium Nanoparticles Protect Lung Tissue from Radiation Damage

in-vivo,

Nor,

30 male Wistar rats

*radioP↑, This study highlights the significant potential of SeNPs as radioprotective agents, showing they mitigate radiation-induced lung damage by preserving tissue integrity and reducing inflammation, consistent with their known antioxidant and anti-inflamm
*Inflam↓,
*antiOx↑,
*Dose↝, SeNPs were administered via intraperitoneal (IP) injection starting 10 days before irradiation, continuing until the day of irradiation. On the tenth day, final doses were given 30 minutes prior to irradiation
*DNAdam↓, SeNPs have attracted considerable interest as radioprotective agents due to their capacity to reduce radiation-induced oxidative stress and DNA damage.[
*ROS↓, By scavenging ROS and enhancing the activity of endogenous antioxidant enzymes such as superoxide dismutase SOD and glutathione peroxidase GPx,
*SOD↑,
*GPx↑,
*Dose↝, predominant dosage of 0.5 mg/kg body weight used in our experiments is consistent with previous studies that have documented its efficacy
*eff↑, combination of SeNPs with other agents, such as fish oil, has been shown to enhance protective effects against liver toxicity induced by radiation and chemotherapy

4611-

SeNPs,

Rad,

Radioprotective Effect of Selenium Nanoparticles: A Mini Review

Review,

Var,

*antiOx↑, The reviewed studies showed that selenium nanoparticles had anti-inflammatory and antioxidant properties.
*Inflam↓,
*radioP↑, Furthermore, there was evidence of efficient radioprotection for the organs examined without significant side effects.
*ROCK1↓, Selenium nanoparticles can scavenge reactive oxygen species (ROS) produced by ionizing radiation, protect normal cells from DNA damage and apoptosis, and increase the radiosensitivity of tumor cells.
*DNAdam↓,
*Apoptosis↓,
*RadioS↑,
*Dose↝, The studies that mainly used a dose of 0.5 mg/kg body weight of SeNPs to assess its radioprotective effects were included for analysis. This dose of SeNPs was effective in preventing kidney and liver damage caused by IR.

4444-

SeNPs,

Antioxidant and Hepatoprotective Efficiency of Selenium Nanoparticles Against Acetaminophen-Induced Hepatic Damage

in-vivo,

LiverDam,

rats

*hepatoP↑, hepatoprotective role of selenium nanoparticles (Nano-Se) against APAP-induced hepatic injury.
*ROS↓, Nano-Se exhibits a protective effect against APAP-induced hepatotoxicity through improved liver function and oxidative stress mediated by catalase, SOD, and GSH and decreases hepatic DNA fragmentation,
*Catalase↑,
*SOD↑,
*GSH↑,
*DNAdam↓,

2406-

SFN,

Sulforaphane and Its Protective Role in Prostate Cancer: A Mechanistic Approach

Review,

Pca,

HK2↓, When TRAMP mice were given 6 μmol/mouse (1 mg/mouse) three times a week for 17–19 weeks, the prostate tumor expression of glycolysis-promoting enzymes such as (HKII), 2 (PKM2) and (LDHA) was decreased by 32–45%
PKM2↓,
LDHA↓,
Glycolysis↓, These results provide evidence that sulforaphane suppresses in vivo glycolysis in prostate cancer cells
LAMP2↑, The study shows that 10–20 μM of sulforaphane significantly increased lysosome-associated membrane protein 2 (LAMP2) in the cell lines
Hif1a↓, sulforaphane has been shown to suppress HIF-1α
DNAdam↓, SFN causes DNA damage and prevents DNA repair in prostate cancer cell
DNArepair↓,
Dose↝, 5 to 100 mg/kg of sulforaphane reduce tumors in animal models [ 5 , 19]. For a 70 kg human, this translates to 350–7000 mg/kg, which is significantly above the upper threshold of tolerable doses

3306-

SIL,

Rad,

Radioprotective and radiosensitizing properties of silymarin/silibinin in response to ionizing radiation

Review,

Var,

radioP↑, Radioprotective and radiosensitizing properties of silymarin/silibinin in response to ionizing radiation
RadioS↑, graphical abstract
TumCMig↓, mechanisms for radiosensitization of silymarin/silibinin have been reported including suppression of migration and invasion of cancer cells, inhibition of angiogenesis, induction of apoptosis and cell cycle arrest, damage to DNA
TumCI↓,
angioG↓,
Apoptosis↑,
DNAdam↓,
ROS↑, increasing the formation of free radicals, and targeting some crucial pathways.
*ROS↓, The combination of silymarin/silibinin and irradiation decreases the toxicities caused by ionizing radiation because of their antioxidant, anti-apoptotic, anti-inflammatory and other properties.
*Inflam↓,

3297-

SIL,

Rad,

Studies on radiation sensitization efficacy by silymarin in colon carcinoma cells

in-vitro,

CRC,

HCT15

in-vitro,

CRC,

RKO

TumCP↓, Silymarin was found to reduce proliferation of the human colon carcinoma cells in a concentration and timedependent manner.
RadioS↑, Moreover, percentage of cell death was also increased in combined treatment (20µg/ml of silymarin + radiation)
TumCCA↑, combination increases the arrest of cells in G 2 /M phase of cell cycle, DNA damage induced decrease in MMP and a decrease of the reactive oxygen species (ROS) levels, which are associated with an increase in cell death
DNAdam↓,
MMP↓,
ROS↓,
*radioP↑, Noteworthy, since silymarin was previously shown to confer protection against radiation in at least some types of normal tissues

5109-

SSE,

Selenium compounds activate ATM-dependent DNA damage response via the mismatch repair protein hMLH1 in colorectal cancer cells

in-vitro,

CRC,

HCT116

ROS↑, We show that hMLH1 complementation sensitizes HCT 116 cells to methylseleninic acid, methylselenocysteine, and sodium selenite via reactive oxygen species
DNAdam↓, and facilitates the selenium-induced oxidative 8-oxoguanine damage, DNA breaks, G2/M checkpoint response, and ATM pathway activation
ATM↑,
eff↓, Pretreatment of the hMLH1-complemented HCT 116 cells with the antioxidant N-acetylcysteine(NAC) or 2,2,6,6-tetramethylpiperidine-1-oxyl or the ATM kinase inhibitor KU55933 suppresses hMLH1-dependent DNA damage response to selenium exposure.
TumCCA↑, Selenium-induced cell cycle arrest and apoptosis in colon cancer cells has been well studied

4610-

SSE,

Rad,

Protection during radiotherapy: selenium

Review,

Var,

*radioP↑, Ebselen, and sodium selenite, emerges as a promising radioprotective agent with demonstrated efficacy across diverse radiation-injured organs, highlighting its significance as an effective and potent antioxidant that affordable for most patients.
*antiOx↑,
*Inflam↓, In short, the antioxidation, anti-inflammatory effect and DNA stabilizing formed the protective effects of selenium against DNA damage induced by radiation
*DNAdam↓,
*lipid-P↓, Se-Met could efficiently inhibit the formation of lipid peroxy radicals, preventing lipid peroxidation
*selenoP↑, primarily enhance the expression of selenoproteins, thus sodium selenite may not be inherently antioxidant until incorporated into selenoproteins with oxidoreductase functions
*GPx1↑, sodium selenite could increase GPx-1 activity in a dose- and time-dependent manner
*BUN↓, 100 µg/day of selenium in the form of sodium selenite or Se-L-Met, blood urea nitrogen (BUN) level of rats significantly decreased.

4614-

SSE,

Rad,

Updates on clinical studies of selenium supplementation in radiotherapy

Review,

Nor,

*toxicity∅, At the dose of selenium used in these studies (200–500 μg/day), selenium supplementation did not reduce the effectiveness of radiotherapy, and no toxicities were reported.
Risk↓, moderate deficiency of selenium has been linked to many conditions, such as an increased risk of cancer, infections and male infertility;
*selenoP↑, Selenium in selenoproteins can reduce oxidative damage and can limit DNA damage
*ROS↓,
*DNAdam↓,
*QoL↑, Most of the studies revealed positive effects of selenium supplementation on the general condition of the patients and their quality of life.
*radioP↑, prevented or reduced the side effects of radiotherapy and did not reduce the effectiveness of radiotherapy or cause any toxicity.
*Dose↝, sodium selenite at doses ranging from 200–500 μg daily by oral administration may offer benefits for head and neck cancer; head and neck cancer with lymphedema; and oral, cervical and uterine cancer patients who undergo radiotherapy and have low sele

2129-

TQ,

doxoR,

Thymoquinone up-regulates PTEN expression and induces apoptosis in doxorubicin-resistant human breast cancer cells

in-vitro,

BC,

MCF-7

25, 50 or 100 µM TQ

ChemoSen↑, TQ greatly inhibits doxorubicin-resistant human breast cancer MCF-7/DOX cell proliferation
PTEN↑, TQ treatment increased cellular levels of PTEN proteins
p‑Akt↓, resulting in a substantial decrease of phosphorylated Akt, a known regulator of cell survival.
TumCCA↑, TQ arrested MCF-7/DOX cells at G2/M phase and increased cellular levels of p53 and p21 proteins.
P53↑,
P21↑,
Apoptosis↑, TQ-induced apoptosis was associated with disrupted mitochondrial membrane potential and activation of caspases and PARP cleavage in MCF-7/DOX cells.
MMP↓,
Casp↑,
cl‑PARP↑,
Bax:Bcl2↑, TQ treatment increased Bax/Bcl2 ratio via up-regulating Bax and down-regulating Bcl2 proteins.
eff↓, PTEN silencing by target specific siRNA enabled the suppression of TQ-induced apoptosis resulting in increased cell survival.
DNAdam↓, TQ treatment arrests MCF-7/DOX Cells in G2/M phase and induces DNA damage
p‑γH2AX↑, time-dependent increase in the phosphorylation of H2AX was observed following TQ treatment
ROS↑, DNA damage caused by TQ induced reactive species and oxidative stress.

4861-

Uro,

Urolithin A improves Alzheimer's disease cognition and restores mitophagy and lysosomal functions

in-vivo,

AD,

mice were treated with UA (200 mg/kg/day) by oral gavage for 5 months, ending at 17 months

three mouse models of AD

*memory↑, Long‐term UA treatment significantly improved learning, memory, and olfactory function in different AD transgenic mice.
*Aβ↓, UA also reduced amyloid beta (Aβ) and tau pathologies and enhanced long‐term potentiation
*toxicity↓, A phase I clinical study confirmed that UA was safe in healthy, sedentary older adults, and that activation of mitochondrial biomarkers in muscle and plasma was observed
*BBB↑, may play a therapeutic role in the brain as it crosses the blood–brain barrier.
*p‑tau↓, UA decreased Aβ accumulation and tau phosphorylation in AD mice
*eff↓, and that the effects disappeared if UA treatment was suspended for 1 month.
*IL1α↓, several proinflammatory cytokines were increased in AD mice and decreased after UA treatment, including Interleukin 1 alpha (IL‐1α), monocyte chemoattractant protein‐1 (MCP‐1)
*MCP1↓,
*MIP‑1α↓, macrophage inflammatory protein‐1 alpha (MIP‐1α), tumor necrosis factor (TNFα), Interleukin 2 (IL‐2)
*TNF-α↓,
*IL2↓,
*SIRT1↓, UA induced sirtuin expression, mitophagy, and decreased DNA damage
*DNAdam↓,
*Dose↝, UA at doses from 250 to 2000 mg in humans 25 and 1–450 mg/kg in mice 80 has been reported to be safe.
*Strength↑, UA increased muscle strength and physical performance in a 6‐min walk test in elderly humans after 4 months of supplementation.
*motorD↑, Other studies reported that UA improved motor activity in the rotarod test and increased total distance traveled and average speed in the open field test in young C57BL/6J mice 82 and 3xTg AD mice
*CTSZ↓, Ctsz was highly expressed in multiple AD transgenic mouse models, and its expression was normalized by UA treatment

4033-

VitB3,

Can nicotinamide riboside protect against cognitive impairment?

in-vivo,

AD,

mouse

*memory↑, Oral supplementation with nicotinamide riboside can inhibit the accumulation of pathological hallmarks of Alzheimer's disease and improve learning and memory in various murine models for dementia
*DNAdam↓, Nicotinamide riboside can also reduce DNA damage, neuroinflammation, apoptosis, and improved hippocampal synaptic plasticity in diabetic mice, and another Alzheimer's disease mouse model.
*Inflam↓,
*Apoptosis↓,
*cognitive↑, The cognitive benefits of nicotinamide riboside in Alzheimer's disease models may be modulated in part by upregulation of proliferator-activated-γ coactivator 1α-mediated β-secretase 1(BACE-1) ubiquitination and degradation, preventing Aβ production
*BACE↓,
*Aβ↓,
*BBB↑, Nicotinamide riboside also maintained blood-brain barrier integrity and maintained the gut microbiota in a mouse model for cerebral small vessel disease and alcohol-induced depression, respectively.
*GutMicro↑,
*eff↑, Oral nicotinamide riboside has been shown to be bioavailable and well tolerated in humans with limited adverse effects compared to other NAD+ precursors.

4032-

VitB3,

Modulation of cGAS-STING Pathway by Nicotinamide Riboside in Alzheimer's Disease

in-vivo,

AD,

*DNAdam↓, reduces senescence of affected cells, attenuates DNA damage and neuroinflammation in the transgenic APP/PS1 murine model of AD.
*Inflam↓,
*other↓, Elevated cGAS-STING observed in the AD mouse brains and human AD fibroblasts was normalized by NR.
*cognitive↑, This intervention also increased mitophagy with improved cognition and behavior in the APP/PS1 mice
*Mood↑,

3104-

VitC,

Pro- and Antioxidant Effects of Vitamin C in Cancer in correspondence to Its Dietary and Pharmacological Concentrations

*antiOx↑, Vitamin C is an antioxidant that may scavenge reactive oxygen species preventing DNA damage and other effects important in cancer transformation
*ROS↓,
*DNAdam↓,
ROS↑, High pharmacological doses of vitamin C may induce prooxidant effects, detrimental for cancer cells.
TET1↑, Vitamin C may change the metabolomic and epigenetic profiles of cancer cells, and activation of ten-eleven translocation (TET) proteins and downregulation of pluripotency factors by the vitamin may eradicate cancer stem cells.
CSCs↓,
HIF-1↓, Vitamin C induces degradation of hypoxia-inducible factor, HIF-1, essential for the survival of tumor cells in hypoxic conditions
BioAv↑, Flavonoids may modulate bioavailability of vitamin C. Animal studies with flavonoid-rich extracts or purified plant flavonoids showed an enhanced uptake of vitamin C when it was administered together with flavonoids
selectivity↑, Chen et al. demonstrated that intravenous administration of ascorbic acid at high concentrations was toxic for many types of cancer cells in xenografts in mice with no effect on normal cells

3128-

VitC,

Vitamin C Mitigates Oxidative Stress and Tumor Necrosis Factor-Alpha in Severe Community-Acquired Pneumonia and LPS-Induced Macrophages

in-vitro,

Nor,

*ROS↓, Vitamin C significantly decreased ROS, DNA damage, TNF-α, and IL-6. Vitamin C inhibited LPS-induced ROS, DNA damage, TNF-α, IL-6, and p38 in macrophages cells.
*DNAdam↓,
*TNF-α↓,
*IL6↓,
*p38↓,

2276-

VitK2,

Vitamin K2 (MK-7) Intercepts Keap-1/Nrf-2/HO-1 Pathway and Hinders Inflammatory/Apoptotic Signaling and Liver Aging in Naturally Aging Rat

in-vivo,

Nor,

rat

*Albumin↑, parallel significant restoration of the serum total protein and albumin by 1.1- and 1.13-fold
*AST↓, VK2 administration reversed this situation, as confirmed by the significant decrease in serum ALT and AST by 0.25- and 0.27-fold
*ALAT↓,
*Keap1↓, significant decrease in Keap-1 mRNA by 0.32-fold
*NRF2↑, significant restoration of the Nrf-2 mRNA level
*HO-1↑,
*COX2↓, VK2 administration to aged animals attenuated hepatic inflammation where hepatic sections from aged-treated rats demonstrated a marked downregulation in COX-2, iNOS and TNF-α
*iNOS↓,
*TNF-α↓,
*TIMP1↓, VK2-treated aged rats showed a significant downregulation in both hepatic TIMP-1 concentration and TGF-β immunostaining compared to the aged untreated control
*TGF-β↓,
*ROS↓, Emerging evidence reported Nrf-2 signaling and VK to play a crucial role in counteracting oxidative stress, DNA damage, senescence and inflammation. These events help in quenching ROS
*DNAdam↓,
*Inflam↓,

Showing Research Papers: 1 to 48 of 48

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 48

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 10, Bil↓, 1, Catalase↑, 6, GPx↑, 4, GPx1↑, 2, GPx4↑, 1, GSH↓, 1, GSH↑, 7, GSR↑, 1, GSTs↑, 2, HO-1↑, 6, Keap1↓, 1, lipid-P↓, 6, lipid-P↑, 1, MDA↓, 2, NQO1↑, 1, NRF2↑, 7, p‑NRF2↑, 1, Prx↑, 1, ROS↓, 28, selenoP↑, 4, SIRT3↑, 1, SOD↑, 8,

Mitochondria & Bioenergetics ⓘ

MMP↑, 1, mtDam↓, 1,

Core Metabolism/Glycolysis ⓘ

ACC↓, 1, ALAT↓, 3, BUN↓, 1, FASN↓, 1, SIRT1↓, 1, SIRT1↑, 2, SREBP1↓, 1,

Cell Death ⓘ

Apoptosis↓, 3, BAX↓, 2, Bax:Bcl2↓, 1, Casp↓, 1, Casp3↓, 2, cl‑Casp3↓, 1, iNOS↓, 2, JNK↓, 1, p38↓, 1,

Transcription & Epigenetics ⓘ

cJun↓, 1, p‑cJun↓, 1, other↓, 2, other↝, 1,

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 38, SIRT6↑, 2,

Proliferation, Differentiation & Cell State ⓘ

cFos↓, 1, ERK↑, 1,

Migration ⓘ

5LO↓, 1, Ca+2↓, 2, Ca+2↝, 1, Ki-67↓, 1, MMP1↓, 1, MMP2↓, 1, MMP2↑, 1, ROCK1↓, 2, TGF-β↓, 1, TIMP1↓, 1, ZO-1↑, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 2,

Barriers & Transport ⓘ

BBB↑, 3,

Immune & Inflammatory Signaling ⓘ

COX2↓, 3, CTSZ↓, 1, ICAM-1↓, 1, IL1↓, 1, IL10↓, 1, IL10↑, 1, IL1α↓, 1, IL1β↓, 1, IL2↓, 1, IL22↓, 1, IL6↓, 5, IL8↓, 1, Imm↑, 1, Inflam↓, 16, MCP1↓, 2, MIP‑1α↓, 1, NF-kB↓, 4, PGE2↓, 1, RANTES↓, 1, TNF-α↓, 8,

Cellular Microenvironment ⓘ

cGAS–STING↓, 1,

Synaptic & Neurotransmission ⓘ

5HT↑, 1, AChE↓, 1, BDNF↑, 2, tau↓, 1, p‑tau↓, 2,

Protein Aggregation ⓘ

Aβ↓, 2, BACE↓, 1, NLRP3↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 2, BioAv↑, 4, BioAv↝, 1, ChemoSen↑, 1, Dose↑, 1, Dose↝, 9, eff↓, 1, eff↑, 7, P450↑, 1, RadioS↑, 1,

Clinical Biomarkers ⓘ

ALAT↓, 3, Albumin↑, 1, ALP↓, 1, AST↓, 3, BG↓, 1, Bil↓, 1, creat↓, 1, GutMicro↑, 2, IL6↓, 5, Ki-67↓, 1,

Functional Outcomes ⓘ

AntiAge↑, 1, AntiCan↑, 4, AntiDiabetic↑, 1, cardioP↑, 4, cognitive↑, 6, hepatoP↑, 5, memory↑, 5, Mood↑, 1, motorD↑, 2, neuroP↑, 7, OS↑, 2, QoL↑, 1, radioP↑, 11, RenoP↑, 1, Sleep↑, 1, Strength↑, 1, toxicity↓, 2, toxicity↝, 1, toxicity∅, 2, Weight↓, 1, Wound Healing↑, 1,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 134

Scientific Paper Hit Count for: DNAdam, DNA damage

9 Radiotherapy/Radiation
5 nicotinamide adenine dinucleotide
4 Lycopene
4 Vitamin B3,Niacin
3 Selenium
3 Selenium NanoParticles
3 Selenite (Sodium)
2 Boron
2 Chemotherapy
2 Silymarin (Milk Thistle) silibinin
2 Vitamin C (Ascorbic Acid)
1 5-Hydroxytryptophan
1 Allicin (mainly Garlic)
1 Ashwagandha(Withaferin A)
1 Astaxanthin
1 Aloe anthraquinones
1 Baicalein
1 Berberine
1 Curcumin
1 Boswellia (frankincense)
1 Cat’s Claw
1 Coenzyme Q10
1 Calorie Restriction Mimetics
1 Ellagic acid
1 Fisetin
1 γ-linolenic acid (Borage Oil)
1 Licorice
1 Moringa oleifera
1 Propolis -bee glue
1 Resveratrol
1 Sulforaphane (mainly Broccoli)
1 Thymoquinone
1 doxorubicin
1 Urolithin
1 Vitamin K2

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:82  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

DNAdam Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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