Database Query Results : Allicin (mainly Garlic), , Cyt‑c

AL, Allicin (mainly Garlic): Click to Expand ⟱
Features:
Garlic (Allium sativum L.) (active ingredient- Allicin, an active sulfer compound).

Allicin — a reactive organosulfur thiosulfinate generated in situ when garlic (Allium sativum) tissue is crushed (alliin → allicin via alliinase). Functionally, it behaves as a short-lived electrophilic “reactive sulfur species” that rapidly modifies cellular thiols (e.g., glutathione and cysteine residues on proteins), producing broad redox and stress-signaling effects. Classification: small-molecule phytochemical (organosulfur thiosulfinate). Standard abbreviation(s): AL (common in Nestronics), “allicin”. Source/origin: freshly crushed raw garlic; allicin is not present in intact cloves and is chemically unstable, converting to other organosulfur metabolites after formation.

Primary mechanisms (ranked):

  1. Thiol reactivity and redox disruption: rapid GSH/protein-thiol modification (S-thioallylation), shifting redox buffering and triggering oxidative/electrophilic stress signaling.
  2. Mitochondrial stress and intrinsic apoptosis (context-dependent): ΔΨm disruption, cytochrome-c release, caspase activation, ER stress/UPR engagement (often downstream of redox stress).
  3. Inflammatory transcriptional suppression (context-dependent): inhibition of NF-κB–linked programs and, in some models, STAT3 signaling.
  4. Acetate metabolism constraint (model-dependent): reversible inhibition of acetyl-CoA synthetase activity (ACS/ACSS), potentially impacting acetate→acetyl-CoA flux under metabolic stress.
  5. Growth and invasion signaling attenuation (model-dependent): PI3K/AKT and MAPK network modulation with downstream effects on EMT/MMPs and angiogenic programs (e.g., HIF-1α/VEGF).

Bioavailability / PK relevance: “Allicin exposure” is dominated by formation conditions and rapid chemical/biologic turnover. Many oral preparations deliver alliin/alliinase that may generate allicin after ingestion; measured systemic allicin is typically transient, while downstream allyl-sulfur metabolites (e.g., allyl methyl sulfide–related products) are more detectable. Cooking/processing and GI conditions substantially change allicin bioequivalence versus crushed raw garlic.

In-vitro vs systemic exposure relevance: Many anticancer cell studies use ~50–300 µM allicin; whether such free allicin concentrations are achievable at tumor sites after dietary/supplement intake is uncertain because of rapid thiol quenching and conversion to other sulfur species. Reported biological effects at lower concentrations may still occur locally (GI lumen/mucosa) or via metabolites, but direct extrapolation from high-µM in-vitro dosing is high-risk.

Clinical evidence status: Predominantly preclinical (cell/animal) for anticancer mechanisms; human data are mixed and often evaluate garlic preparations rather than purified allicin, with outcomes confounded by formulation-dependent “allicin bioequivalence” and co-occurring organosulfur compounds (e.g., DADS/DATS/SAMC). Cancer-therapeutic evidence remains inconclusive.

DADS (diallyl disulfide is a sulfur-based anticancer drug generated from garlic)
Summary:
- Four main organic sulfides in garlic, diallyl disulfide (DADS), diallyl trisulfide (DATS), S-allylmercaptocysteine (SAMC) and allicin.
- Reversible inhibitor of ACSS2.
- may inhibit NF-κB signaling
- induce oxidative stress in cancer cells by generating ROS
- might downregulate STAT3 activation
- Inconclusive evidence for cancer treatment.
- may inhibit platelet aggregation
Allicin is a reactive sulfur species (RSS) [23] with oxidizing properties, and it is able to oxidize thiols in cells, e.g., glutathione and cysteine residues in proteins.
-Allicin is not present in intact garlic; rather, it is formed when garlic is chopped or crushed. -Using crushed or chopped raw garlic or adding garlic at the end of the cooking process (after the heat is reduced) can help preserve its potential allicin content.
"Consumption of alliinase-inhibited cooked garlic was found to give higher than expected allicin bioequivalence, with AMS formation being about 30% (roasted garlic) or 16% (boiled garlic) that of crushed raw garlic."

-Allicin is not present in intact garlic.
-It's formed enzymatically when alliin (a sulfur-containing amino acid) is converted by alliinase when garlic is chopped or crushed.Best consumed raw immediately after crushing (wait 5–10 min before consuming for full conversion)
-Allicin is unstable, degrading within hours into other sulfur compounds (like diallyl disulfide).

-Note half-life reports vary 2.5-90hrs?.
-moderately water-soluble but rapidly degrades/quenched (especially with thiols), so aqueous solutions have limited practical stability : BioAv


Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, UPR↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓
- Raises AntiOxidant defense in Normal Cells: NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- PI3K/AKT(Inhibition), JAK/STATs, Wnt/β-catenin, AMPK, MAPK/ERK, and JNK.
- inhibit Growth/Metastases : EMT↓, MMP2↓, MMP9↓, VEGF↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓(not commonly listed as inhibitor), DNMT1↓, P53↑, HSP↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, FAK↓, ERK↓,
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, EGFR↓,
- inhibits Cancer Stem Cells : CSC↓,
- Others: PI3K↓, AKT↓, STAT3, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,
- Selectivity: Cancer Cells vs Normal Cells

Allicin has been reported to exhibit a range of effects, including:
Antimicrobial activity: 10-50 μM
Antioxidant activity: 10-100 μM
Anti-inflammatory activity: 20-50 μM
Anticancer activity: 50-100 μM or (50–300uM) (2–5 mg allicin per kilogram of body weight per day)
Cardiovascular health: 20-50 μM

Approximate μM concentrations of allicin that can be achieved:
1 clove of garlic (3g): approximately 10-50 μM of allicin
single clove of garlic may yield about 5–9 mg of allicin,
1 tablespoon of minced garlic (15g): approximately 50-150 μM of allicin
1 cup of chopped garlic (100g): approximately 200-500 μM of allicin
1 tablespoon of chopped garlic chives (15g): approximately 5-20 μM of allicin
1 cup of chopped garlic chives (100g): approximately 20-50 μM of allicin
1 ounce (28g) of garlic microgreens: approximately 50-200 μM of allicin
1 cup of garlic microgreens (100g): approximately 200-500 μM of allicin
1 ounce (28g) of garlic chive microgreens: approximately 20-50 μM of allicin
1 cup of garlic chive microgreens (100g): approximately 50-100 μM of allicin

Allicin is a bioactive compound derived from garlic that has garnered significant interest for its potential anticancer properties through multiple mechanisms, including antioxidant activity, induction of apoptosis, cell cycle arrest, and modulation of key signaling pathways. While regular dietary intake of garlic is associated with cancer prevention benefits, allicin is also being explored as an adjunct to conventional cancer treatments.

Available in supplement tablet/capsule form for example at 2000mg (fresh bulb equilvalent)
IC50 of normal cells it >160mg/mL (large selectivity).
IC50 might be about 12-30ug/ml (approximately 62-185 µM) (which is about 30-90 grams of garlic consumption).
This makes it difficult to consume enough supplements to achieve that level.

Pathways:

ROS Generation and Oxidative Stress (inducing)
• ROS generation is often considered a primary trigger that feeds into downstream pathways (e.g., MAPK activation, mitochondrial membrane permeabilization).
Mitochondrial (Intrinsic) Apoptotic Pathway
• ROS-induced mitochondrial damage can lead to the release of cytochrome c and subsequent activation of caspases (e.g., caspase-9 and caspase-3).
NF-κB Signaling Inhibition (block)
Modulation of MAPK Pathways (e.g., p38 MAPK and JNK)
• ROS generation by allicin can activate stress-responsive kinases such as p38 MAPK and c-Jun N-terminal kinase (JNK).
Inhibition of PI3K/Akt Pathway
ROS levels and PI3K/Akt signaling, with increased oxidative stress often correlating with reduced Akt phosphorylation and activity.

At lower doses, allicin may lead to a modest increase in ROS levels that the cell’s antioxidant defenses (e.g., glutathione, superoxide dismutase) can manage

Allicin (Garlic) — mechanistic axes relevant to oncology

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Thiol chemistry and redox buffering GSH↓, protein thiols modified; ROS↑ (dose-dependent) Adaptive buffering often stronger; ROS↔/↑ (context-dependent) P Electrophilic/thiol stress that re-wires signaling Central “first-contact” mechanism: allicin rapidly reacts with cysteine/GSH, so many downstream pathway changes are secondary to thiol stress.
2 Mitochondria and intrinsic apoptosis ΔΨm↓, Cyt-c↑, Caspase↑, cl-PARP↑ Typically less apoptosis at matched doses (selectivity varies) R Pro-apoptotic stress execution Frequently downstream of rank #1; selectivity can reflect baseline redox fragility and metabolic state.
3 ER stress and UPR ER stress↑, UPR↑ (model-dependent) UPR↔/↑ (context-dependent) R Proteostasis stress amplification Can couple to Ca²⁺ release, apoptosis, and inflammatory signaling changes.
4 Ca²⁺ signaling Ca²⁺↑ (model-dependent) Ca²⁺↔/↑ (context-dependent) R Stress coupling to mitochondria/ER Often reported as part of the ER–mitochondria stress axis rather than a primary target.
5 NF-κB inflammatory axis NF-κB↓; cytokine programs↓ (context-dependent) Inflammatory tone↓ (context-dependent) G Anti-inflammatory transcriptional suppression May be beneficial in tumor-promoting inflammation contexts; also relevant to platelet/vascular biology.
6 STAT3 signaling STAT3↓ (model-dependent) STAT3↔ (context-dependent) G Reduced survival/proliferation programs Evidence is model-specific; frequently downstream of redox/inflammation modulation.
7 NRF2 antioxidant response NRF2↓ or maladaptive NRF2 response (context-dependent) NRF2↑ (context-dependent) G Differential stress adaptation Reported “cancer vs normal” divergence is plausible but not universal; strongly dose/model dependent.
8 Acetate to acetyl-CoA metabolism ACS/ACSS activity↓ (model-dependent) ACS/ACSS activity↓ (context-dependent) R Limits acetate utilization under stress Primary biochemical evidence exists for acetyl-CoA synthetase inhibition by allicin; translation to tumor-selective ACSS2 targeting is uncertain without exposure confirmation.
9 PI3K/AKT and MAPK network PI3K/AKT↓, ERK/JNK↔/↓ (model-dependent) ↔ (context-dependent) G Reduced growth/survival signaling Commonly reported but typically secondary to upstream stress/redox effects.
10 HIF-1α and angiogenesis HIF-1α↓, VEGF↓ (model-dependent) ↔ (context-dependent) G Anti-angiogenic signaling shift Most supportive data are preclinical; dependent on hypoxia models and dosing.
11 EMT, migration, invasion EMT↓, MMPs↓ (model-dependent) ↔ (context-dependent) G Reduced invasive phenotype Usually downstream of PI3K/MAPK/inflammation rewiring and/or oxidative stress–driven cytostasis.
12 Radiosensitization and chemosensitization Sensitization↑ (context-dependent) Protection↔/↑ (context-dependent) G Stress-based therapeutic interaction Potential bidirectionality: pro-oxidant sensitization in tumors vs antioxidant adaptation in normal tissues depends on schedule and formulation.
13 Clinical Translation Constraint Chemical instability; rapid thiol quenching; formulation-dependent “allicin bioequivalence”; uncertain tumor-site free-allicin exposure; many in-vitro studies use high µM levels; human cancer outcomes largely from heterogeneous garlic preparations rather than purified allicin. Primary constraint is exposure control, not target plausibility.


Cyt‑c, cyt-c Release into Cytosol: Click to Expand ⟱
Source:
Type:
Cytochrome c
** The term "release of cytochrome c" ** an increase in level for the cytosol.
Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis.

The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis.
In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death.
Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation.
Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol.
The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death.

On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer.
On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells.
Overexpressed in Breast, Lung, Colon, and Prostrate.
Underexpressed in Ovarian, and Pancreatic.
Scientific Papers found: Click to Expand⟱
2660- AL,    Allicin: A review of its important pharmacological activities
- Review, AD, NA - Review, Var, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, It showed neuroprotective effects, exhibited anti-inflammatory properties, demonstrated anticancer activity, acted as an antioxidant, provided cardioprotection, exerted antidiabetic effects, and offered hepatoprotection.
AntiCan↑,
*antiOx↑,
*cardioP↑, This vasodilatory effect helps protect against cardiovascular diseases by reducing the risk of hypertension and atherosclerosis.
*hepatoP↑,
*BBB↑, This allows allicin to easily traverse phospholipid bilayers and the blood-brain barrier
*Half-Life↝, biological half-life of allicin is estimated to be approximately one year at 4°C. However, it should be noted that its half-life may differ when it is dissolved in different solvents, such as vegetable oil
*H2S↑, allicin undergoes metabolism in the body, leading to the release of hydrogen sulfide (H2S)
*BP↓, H2S acts as a vasodilator, meaning it relaxes and widens blood vessels, promoting blood flow and reducing blood pressure.
*neuroP↑, It acts as a neuromodulator, regulating synaptic transmission and neuronal excitability.
*cognitive↑, Studies have suggested that H2S may enhance cognitive function and protect against neurodegenerative diseases like Alzheimer's and Parkinson's by promoting neuronal survival and reducing oxidative stress.
*neuroP↑, various research studies suggest that the neuroprotective mechanisms of allicin can be attributed to its antioxidant and anti-inflammatory properties
*ROS↓,
*GutMicro↑, may contribute to the overall health of the gut microbiota.
*LDH↓, Liu et al. found that allicin treatment led to a significant decrease in the release of lactate dehydrogenase (LDH),
*ROS↓, allicin's capacity to lower the production of reactive oxygen species (ROS), decrease lipid peroxidation, and maintain the activities of antioxidant enzymes
*lipid-P↓,
*antiOx↑,
*other↑, allicin was found to enhance the expression of sphingosine kinases 2 (Sphk2), which is considered a neuroprotective mechanism in ischemic stroke
*PI3K↓, allicin downregulated the PI3K/Akt/nuclear factor-kappa B (NF-κB) pathway, inhibiting the overproduction of NO, iNOS, prostaglandin E2, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha induced by interleukin-1 (IL-1)
*Akt↓,
*NF-kB↓,
*NO↓,
*iNOS↓,
*PGE2↓,
*COX2↓,
*IL6↓,
*TNF-α↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
*MPO↓, Furthermore, allicin significantly decreased tumor necrosis factor-alpha (TNF-α) levels and myeloperoxidase (MPO) activity, indicating its neuroprotective effect against brain ischemia via an anti-inflammatory pathway
*eff↑, Allicin, in combination with melatonin, demonstrated a marked reduction in the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap-1), and NF-κB genes in rats with brain damage induced by acryl
*NRF2↑, Allicin treatment decreased oxidative stress by upregulating Nrf2 protein and downregulating Keap-1 expression.
*Keap1↓,
*TBARS↓, It significantly reduced myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS) levels,
*creat↓, and decreased blood urea nitrogen (BUN), creatinine, LDH, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) levels.
*LDH↓,
*AST↓,
*ALAT↓,
*MDA↓,
*SOD↑, Allicin also increased the activity of superoxide dismutase (SOD) as well as the levels of glutathione S-transferase (GST) and glutathione (GSH) in the liver, kidneys, and brain
*GSH↑,
*GSTs↑,
*memory↑, Allicin has demonstrated its ability to improve learning and memory deficits caused by lead acetate injury by promoting hippocampal astrocyte differentiation.
chemoP↑, Allicin safeguards mitochondria from damage, prevents the release of cytochrome c, and decreases the expression of pro-apoptotic factors (Bax, cleaved caspase-9, cleaved caspase-3, and p53) typically activated by cisplatin
IL8↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
Cyt‑c↑, In addition, allicin was reported to induce cytochrome c, increase expression of caspase 3 [86], caspase 8, 9 [82,87], caspase 12 [80] along with enhanced p38 protein expression levels [81], Fas expression levels [82].
Casp3↑,
Casp8↑,
Casp9↑,
Casp12↑,
p38↑,
Fas↑,
P53↑, Also, significantly increased p53, p21, and CHK1 expression levels decreased cyclin B after allicin treatment.
P21↑,
CHK1↓,
CycB/CCNB1↓,
GSH↓, Depletion of GSH and alterations in intracellular redox status have been found to trigger activation of the mitochondrial apoptotic pathway was the antiproliferative function of allicin
ROS↑, Hepatocellular carcinoma (HCC) cells were sensitised by allicin to the mitochondrial ROS-mediated apoptosis induced by 5-fluorouracil
TumCCA↑, According to research findings, allicin has been shown to decrease the percentage of cells in the G0/G1 and S phases [87], while causing cell cycle arrest at the G2/M phase
Hif1a↓, Allicin treatment was found to effectively reduce HIF-1α protein levels, leading to decreased expression of Bcl-2 and VEGF, and suppressing the colony formation capacity and cell migration rate of cancer cells
Bcl-2↓,
VEGF↓,
TumCMig↓,
STAT3↓, antitumor properties of allicin have been attributed to various mechanisms, including promotion of apoptosis, inhibition of STAT3 signaling
VEGFR2↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,

2656- AL,    Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics
- in-vitro, Park, PC12
*antiOx↑, Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-oxidative and anti-apoptotic activities in in vitro and in vivo studies.
*Apoptosis↓, allicin treatment significant increased cell viability, and decreased LDH release and apoptotic cell death after 6-OHDA exposure
*LDH↓,
ROS↓, Allicin also inhibited ROS generation
*lipid-P↓, reduced lipid peroxidation and preserved the endogenous antioxidant enzyme activities.
*mtDam↓, These protective effects were associated with suppressed mitochondrial dysfunction,
*MMP↓, as evidenced by decreased MMP collapse and cytochrome c release,
*Cyt‑c↓,
*ATP∅, preserved mitochondrial ATP synthesis,
*Ca+2↝, and the promotion of mitochondrial Ca(2+) buffering capacity
*neuroP↑, allicin treatment can exert protective effects against PD related neuronal injury through inhibiting oxidative stress and mitochondrial dysfunction with dynamic changes.

2655- AL,    Allicin and Digestive System Cancers: From Chemical Structure to Its Therapeutic Opportunities
- Review, GC, NA
TGF-β↓, Allicin can reduce the expression of TGF-2 and its receptor after entering directly into gastric cancer cell
cycD1/CCND1↓, followed by not only downexpression of cyclinD1, cyclinE, and cyclin-dependent kinase (CDK),
cycE/CCNE↓,
CDK1↓, cyclin-dependent kinase (CDK)
DNAdam↑, but also causing DNA damage and generating ROS
ROS↑,
BAX↑, Allicin increases the levels of Bax (proapoptotic protein), Bcl-2 (antiapoptotic protein), and JNK
JNK↑,
MMP↓, through reduction in outer mitochondrial membrane potential
p38↑, allicin induces p38 mitogen that could induce the protein kinase (MAPK) and then increase the expression of Fas binding to Fas ligand (Fas L) and finally activate death pathway through activation of cyt C and caspase-8.
MAPK↑,
Fas↑,
Cyt‑c↑,
Casp8↑,
PARP↑, allicin makes caspase-dependent apoptosis through elevating PARP, caspase-3 and caspase-9, which are mediated by enhanced discharging of mitochondria cyt C to the cytosol.
Casp3↑,
Casp9↑,
Ca+2↑, allicin induces apoptosis via increasing the amounts of free Ca2+, ER stress.
ER Stress↑,
P21↑, generating ROS to produce p21 and phospho-p53 (Ser15).
CDK2↓, Then p21 suppressed the CDK-4/6/cyclinD complex, P21-PCNA, P21-CDK2, and subsequently reduced cdk1/cyclinB1 complex for G2/M phase cell cycle arrest
CDK6↑,
TumCCA↑,
CDK4↓, Then p21 suppressed the CDK-4/6/cyclinD complex

5356- AL,    Therapeutic role of allicin in gastrointestinal cancers: mechanisms and safety aspects
- Review, GC, NA
Apoptosis↑, induction of apoptosis, inhibition of proliferation, and disruption of cancer cell signaling pathways, including the MAPK, PI3K/AKT, and NF-κB pathways.
TumCP↓,
MAPK↓,
PI3K↓,
Akt↓,
NF-kB↓,
AntiCan↑, Allicin and its other derivatives, such as diallyl disulfide (DADS) and ajoene, have been found to have strong anticancer potential both in vitro and in vivo.
ChemoSen↑, effectiveness of allicin in augmenting conventional chemotherapy and retarding tumor growth proves that allicin is one of the most efficient complementary therapies.
TumCCA↑, In liver cancer, allicin has been shown to mediate cell cycle arrest and apoptosis
Apoptosis↑,
BioAv↑, Allicin (diallyl thiosulfinate) is a compound that is generated when a garlic clove is crushed
selectivity↑, Furthermore, it has no influence on the growth of healthy intestinal cells when it causes stomach cancer cells to undergo apoptosis
TGF-β↓, Allicin can reduce the production of TGF-β2 and its receptor after directly entering gastric cancer cells.
ROS↑, It induces oxidative stress by generating reactive oxygen species (ROS), leading to DNA damage and activation of key apoptotic mediators such as phospho-p53 and p21 [81].
DNAdam↑,
p‑P53↑,
P21↑,
cycD1/CCND1↓, Additionally, cyclin D1, cyclin E, and cyclin-dependent kinases (CDKs) can all be inhibited by allicin.
cycE/CCNE↓,
CDK4↓, suppressing the CDK-4/6/cyclin D complex
CDK6↓,
MMP↓, By lowering the outer mitochondrial membrane potential (MMP), allicin raises levels of nuclear factor kappa B (NF-κB), the proapoptotic protein Bax, while decreasing the antiapoptotic protein Bcl-2, which leads to apoptosis.
NF-kB↑,
BAX↑,
Bcl-2↓,
ER Stress↑, cellular effects of allicin, including its role in inducing ER stress
Casp↑, enhancing caspase activation and apoptosis-inducing factor (AIF)-mediated cell death.
AIF↑,
Fas↑, increasing Fas receptor expression and its binding to Fas ligand (FasL), leading to apoptosis through caspase-8 and cytochrome c activation.
Casp8↑,
Cyt‑c↑,
cl‑PARP↑, leading to poly (ADP-ribose) polymerase (PARP) cleavage and DNA fragmentation.
Ca+2↑, allicin elevates intracellular free Ca2⁺ levels, causing endoplasmic reticulum (ER) stress, which plays a critical role in apoptosis induction
*NRF2↑, by activating the Nrf2 pathway via KLF9, allicin protects against arsenic trioxide-induced liver damage,
*chemoP↑, Additionally, allicin has shown promise in reducing hepatotoxicity caused by tamoxifen (TAM), a commonly used treatment for hormone-dependent breast cancer
*GutMicro↑, Shi et al. [85] found that allicin can ameliorate high-fat diet-induced obesity in mice by altering their gut microbiome.
CycB/CCNB1↑, DATS impaired cell survival in the G2 phase by significantly upregulating cyclins A2 and B1.
H2S↑, DATS can also react with the cellular thiol glutathione to create H2S gas, which can control several other cellular functions [79].
HIF-1↓, allicin treatment (40 µg/ml) for NSCLC lowers the expression of HIF-1 and HIF-2 in hypoxic cells [73]
RadioS↑, Allicin has been shown to increase the sensitivity of X-ray radiation therapy in colorectal cancer, presumably by suppressing the levels of NF-κB, IKKβ mRNA, p-NF-κB, and p-IKKβ protein expression in vitro and in vivo

245- AL,    Allicin: a promising modulator of apoptosis and survival signaling in cancer
- Review, Var, NA
Fas↑,
Bcl-2↓,
BAX↑,
PI3k/Akt/mTOR↝, Allicin can inhibit excessive autophagy by activating the PI3K/Akt/mTOR and MAPK/ERK/mTOR signaling pathways.
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↓,
*toxicity↓, Allicin-loaded nano-formulations efficiently induce apoptosis in cancer cells while minimizing toxicity to normal cells
Cyt‑c↑, allicin induces the release of cytochrome c from the mitochondria

254- AL,    Allicin and Cancer Hallmarks
- Review, Var, NA
NRF2⇅, 40 nM
BAX↑,
Bcl-2↓,
Fas↑,
MMP↓,
Bax:Bcl2↑,
Cyt‑c↑,
Casp3↑,
Casp12↑,
GSH↓, Allicin can easily penetrate the cell membrane and react with the cellular thiol to transiently deplete the intracellular GSH level, inducing the inhibition of cell cycle progression and growth arrest [98].
TumCCA↑,
ROS↑, An in vitro study indicated that allicin encourages oxidative stress and autophagy in Saos-2 and U2OS (osteosarcoma cells) by modulating the MALATI-miR-376a-Wnt and β-catenin pathway [99].
antiOx↓, As an antioxidant phytochemical, it scavenges reactive oxygen species (ROS) and protects cells from oxidative DNA damage [34].

251- AL,    Inhibition of allicin in Eca109 and EC9706 cells via G2/M phase arrest and mitochondrial apoptosis pathway
- in-vitro, ESCC, Eca109 - in-vitro, ESCC, EC9706 - in-vivo, NA, NA
Apoptosis↑,
P53↑,
P21↑,
CHK1↑,
CycB/CCNB1↓,
BAX↑,
Casp3↑,
Casp9↑,
Cyt‑c↑, allicin treatment resulted in Cyt c release from the mitochondria to the cytosol.

241- AL,    Role of p38 MAPK activation and mitochondrial cytochrome-c release in allicin-induced apoptosis in SK-N-SH cells
- in-vitro, neuroblastoma, SK-N-SH
Casp3↑,
Casp9↑,
p38↑,
MAPK↑,
Cyt‑c↑, mitochondrial release of cytochrome-c
Apoptosis↑, allicin induced a significant apoptosis compared with the control group

239- AL,    Allicin induces apoptosis in gastric cancer cells through activation of both extrinsic and intrinsic pathways
- in-vitro, GC, SGC-7901
Apoptosis↑,
Cyt‑c↑, induced cytochrome c release from the mitochondria
Casp3↑,
Casp8↑,
Casp9↑,
BAX↑,
Fas↑,
tumCV↓, 30ug/ml allicin treatment for 48 h reduced tumor cell viability by 70%
DNAdam↑, such as DNA damage, oxidative stress and heat shock proteins
ROS↑,
Telomerase↓, Allicin was shown to induce apoptosis in gastric cancer cells, partly by decreased telomerase activity (21).


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   GSH↓, 2,   NRF2⇅, 1,   ROS↓, 1,   ROS↑, 5,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   MMP↓, 3,  

Core Metabolism/Glycolysis ⓘ

H2S↑, 1,   PI3k/Akt/mTOR↝, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↓, 1,   Apoptosis↑, 5,   BAX↑, 6,   Bax:Bcl2↑, 1,   Bcl-2↓, 4,   Casp↑, 1,   Casp12↑, 2,   Casp3↑, 7,   Casp8↑, 5,   Casp9↑, 6,   Cyt‑c↑, 8,   Fas↑, 6,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 2,   p38↑, 3,   Telomerase↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 2,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   CHK1↑, 1,   DNAdam↑, 3,   P53↑, 2,   p‑P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   CDK4↓, 2,   CycB/CCNB1↓, 2,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 2,   P21↑, 4,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,   STAT3↓, 1,  

Migration ⓘ

Ca+2↑, 2,   p‑FAK↓, 1,   TGF-β↓, 2,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

HIF-1↓, 1,   Hif1a↓, 1,   VEGF↓, 1,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL8↓, 1,   NF-kB↓, 1,   NF-kB↑, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,   CDK6↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 1,   RadioS↑, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   chemoP↑, 1,  
Total Targets: 67

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   GSH↑, 1,   GSTs↑, 1,   Keap1↓, 1,   lipid-P↓, 2,   MDA↓, 1,   MPO↓, 1,   NRF2↑, 2,   ROS↓, 2,   SOD↑, 1,   TBARS↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP∅, 1,   MMP↓, 1,   mtDam↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   H2S↑, 1,   LDH↓, 3,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↓, 1,   Cyt‑c↓, 1,   iNOS↓, 1,  

Transcription & Epigenetics ⓘ

other↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,  

Migration ⓘ

Ca+2↝, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL6↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   BP↓, 1,   creat↓, 1,   GutMicro↑, 2,   IL6↓, 1,   LDH↓, 3,  

Functional Outcomes ⓘ

cardioP↑, 1,   chemoP↑, 1,   cognitive↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 3,   toxicity↓, 1,  
Total Targets: 48

Scientific Paper Hit Count for: Cyt‑c, cyt-c Release into Cytosol
9 Allicin (mainly Garlic)
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#:27  Target#:77  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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