Database Query Results : Selenite (Sodium), ,

SSE, Selenite (Sodium): Click to Expand ⟱

Features:

Sodium Selenite - is inorganic selenium in the selenite oxidation state (Se⁴⁺)
Sodium selenite is produced industrially from selenium metal, which itself is obtained as a by-product of copper refining.

Mechanistic distinction from Selenium:
-Selenite reacts with GSH → GS–Se–SG intermediates
-Generates superoxide, H₂O₂
-Exploits cancer cells’ elevated basal oxidative stress
-Normal cells neutralize it more effectively (higher redox reserve)

Both the uptake and processing of selenium has recently shown to be upregulated in subsets of cancer cells
 due to their increased expression of xCT transporter
The more a tumor depends on xCT, the more toxic selenite becomes. High xCT Also Increases SSE Toxicity. High xCT increases intracellular thiols, which increases SSE chemical trapping, redox cycling, and cytotoxic impact.

Sodium selenite might protect against toxicity of AgNPs. also here

SSE and cancer

Rank	Pathway / Target Axis	Direction	Primary Effect	Notes / Cancer Relevance	Ref
1	Redox cycling with thiols (superoxide generation)	↑ O2•− / ↑ ROS	Acute oxidative stress	Defines sodium selenite anticancer mechanism in many models: early superoxide rise precedes mitochondrial apoptotic events	(ref)
2	Glutathione buffering (GSH pool)	↓ GSH	Loss of redox buffering	Work in hepatoma models demonstrates GSH’s key role in selenite-driven oxidative stress and apoptosis	(ref)
3	Mitochondrial integrity (ΔΨm)	↓ ΔΨm	Mitochondrial dysfunction	Sequential mechanism shown: superoxide rise → mitochondrial depolarization	(ref)
4	Intrinsic apoptosis (cytochrome c → Caspase-9/3)	↑ cytochrome c release / ↑ Caspase-9/3	Programmed cell death	Same sequential model shows cytochrome c release followed by caspase-9 and caspase-3 activation	(ref)
5	ER stress / UPR (PERK → eIF2α → ATF4)	↑ PERK/eIF2α/ATF4	Proteotoxic stress signaling	ER-stress module is shown as a core driver in selenite-induced autophagy→apoptosis progression	(ref)
6	Stress MAPK (p38) as switch control	↑ p38 activation	Signal switching (autophagy → apoptosis)	Mechanistic evidence for p38 participating in the selenite-driven transition toward apoptosis	(ref)
7	p53 activation (stress response)	↑ p53 phosphorylation (Ser15)	Facilitates apoptosis programs	NB4 leukemia model: selenite induces p53 Ser15 phosphorylation via p38/ERK in the autophagy–apoptosis switch context	(ref)
8	DNA damage response (ATM-dependent signaling)	↑ ATM-dependent DDR	Checkpoint activation & death signaling	Selenium compounds (including selenite contexts) activate ATM-dependent DNA damage response signaling in colorectal cancer models	(ref)
9	PI3K–AKT axis linked to autophagy/apoptosis balance	↓ PI3K/Akt (functional axis) / ↓ protective autophagy	Apoptosis sensitization	NB4 leukemia: sodium selenite increases apoptosis by autophagy inhibition through PI3K/Akt	(ref)
10	NF-κB signaling	↓ NF-κB	Reduced anti-apoptotic transcription	Mechanistic study: sodium selenite induces ROS-mediated inhibition of NF-κB with downstream shift toward apoptosis	(ref)
11	Angiogenesis signaling (VEGF)	↓ VEGF expression	Reduced vascular support signals	Prostate cancer PC3 model: sodium selenite inhibits expression of VEGF (and related inflammatory/pro-growth factors) in the tested context	(ref)
12	Ferroptosis (iron-dependent oxidative death)	↑ ferroptosis	Non-apoptotic oxidative death modality	Paper explicitly reports sodium selenite as an inducer of ferroptosis across multiple human cancer cell types	(ref)

Table to compare Sodium Selenite to SeNPs
-Sodium selenite → chemical oxidant (thiol attack → ROS shock).
-SeNPs → engineered redox stressor (signaling-level control, broader window).
-Selenomethionine / Se-yeast → redox buffer & selenium storage form (often protective to cancer cells, especially when oxidative stress is a therapeutic goal).

Dimension	Sodium Selenite (Na2SeO3)	Selenium Nanoparticles (SeNPs)	Selenomethionine / Se-Yeast
Primary mechanistic class	Direct redox-disrupting agent	Controlled redox modulator / signaling perturbator	Nutritional selenium reservoir / selenoprotein precursor
Initial molecular interaction	Rapid reaction with cellular thiols (GSH, Trx, protein –SH)	Cellular uptake → gradual selenium release or surface redox effects	Nonspecific incorporation into proteins in place of methionine
ROS generation	↑↑ acute, non-buffered ROS burst	↑ mild–moderate, sustained ROS	↓ or ↔ (antioxidant bias)
Glutathione (GSH) system	↓↓ GSH depletion	↔ or mild ↓ (context-dependent)	↑ GSH recycling via GPX support
Redox selectivity (cancer vs normal)	Limited; toxicity threshold close to efficacy	Improved tumor selectivity window	Poor for cancer killing; favors normal-cell protection
Mitochondrial integrity (ΔΨm)	↓↓ rapid depolarization	↓ gradual, dose-dependent disruption	↔ or ↑ mitochondrial protection
Dominant cell-death pathways	Intrinsic apoptosis ± necrosis (high dose)	Apoptosis ± ferroptosis ± autophagy-related death	None (cytoprotective)
ER stress / UPR (PERK–CHOP)	↑ strong, early activation	↑ moderate, delayed activation	↓ ER stress via antioxidant capacity
DNA damage response	↑ oxidative DNA lesions (ATM/ATR)	↑ low–moderate, secondary to ROS	↓ DNA damage; improved repair environment
PI3K–AKT survival signaling	↓ secondary to oxidative collapse	↓ reported in multiple tumor models	↔ or ↑ survival signaling
NF-κB / inflammatory signaling	↓ via redox inhibition	↓ selectively; anti-inflammatory bias	↓ chronic inflammation (protective)
Ferroptosis involvement	Minor / indirect	↑ lipid peroxidation; GPX4 modulation	↓↓ ferroptosis risk (GPX4 support)
Autophagy	↑ early (protective) → collapse	↑ contributory to tumor suppression	↔ homeostatic maintenance
Angiogenesis (VEGF)	↓ at cytotoxic doses	↓ at lower, tolerated doses	↔ or mild ↓ (indirect)
Immune compatibility	Poor at anticancer doses	Moderate–good; often immune-supportive	High; supports immune competence
Pharmacologic control	Poor (steep dose–toxicity curve)	High (size, coating, release tunable)	Low (slow turnover, storage form)
Normal tissue tolerance	Low	Moderate–high	High
Overall cancer relevance	Potent but hazardous cytotoxic agent	Balanced anticancer redox modulator	Generally counterproductive for direct cancer killing
Overall therapeutic profile	Potent but narrow safety margin	Lower acute potency, broader usable window

Scientific Papers found: Click to Expand⟱

4434-

AgNPs,

SSE,

Sodium Selenite Ameliorates Silver Nanoparticles Induced Vascular Endothelial Cytotoxic Injury by Antioxidative Properties and Suppressing Inflammation Through Activating the Nrf2 Signaling Pathway

vitro+vivo,

Nor,

"highlight2" >*ROS↓, "highlight2" >*Inflam↓, "highlight2" >*NLRP3↓, "highlight2" >*NF-kB↓, "highlight2" >*NRF2↑, "highlight2" >*HO-1↑, "highlight2" >*toxicity↓,

4714-

Se,

SSE,

SeNPs,

Selenium in cancer management: exploring the therapeutic potential

Review,

Var,

"highlight2" >Risk↓, "highlight2" >*BioAv↑, "highlight2" >eff↝, "highlight2" >*ROS↓, "highlight2" >MMP↓, "highlight2" >ROS↑, "highlight2" >P53↑, "highlight2" >*toxicity↓, "highlight2" >TumCP↓, "highlight2" >Casp↑, "highlight2" >Apoptosis↑,

4459-

SeNPs,

VitC,

SSE,

Nano and mesosized selenium and its synthesis using the ascorbic acid route

"highlight2" >*eff↑, "highlight2" >*Dose↝, "highlight2" >*Dose↝,

5082-

SSE,

Rationale for the treatment of cancer with sodium selenite

Review,

Var,

"highlight2" >Risk↑, "highlight2" >antiOx↑, "highlight2" >ROS↑, "highlight2" >Imm↑, "highlight2" >NK cell↑, "highlight2" >angioG↓, "highlight2" >toxicity↓,

5088-

SSE,

Superoxide-mediated ferroptosis in human cancer cells induced by sodium selenite

in-vitro,

BC,

MCF-7

in-vitro,

GBM,

U87MG

in-vitro,

Pca,

PC3

in-vitro,

Cerv,

HeLa

in-vitro,

GBM,

A172

"highlight2" >Ferroptosis↑, "highlight2" >ROS↑, "highlight2" >Iron↑, "highlight2" >xCT↓, "highlight2" >GSH↓, "highlight2" >GPx4↓, "highlight2" >lipid-P↑, "highlight2" >TumCP↓, "highlight2" >selectivity↑,

5087-

SSE,

Sodium Selenite Alleviates Breast Cancer-Related Lymphedema Independent of Antioxidant Defense System

Trial,

BC,

 five sessions of 0.9% saline and 500 μg sodium selenite (Selenase®) IV injections

double-blind, controlled trial was conducted on 26 participants

"highlight2" >eff↑, "highlight2" >Inflam↓, "highlight2" >Imm↑, "highlight2" >ROS↑, "highlight2" >*NK cell↑,

5086-

SSE,

Sodium Selenite Induces Superoxide-Mediated Mitochondrial Damage and Subsequent Autophagic Cell Death in Malignant Glioma Cells

in-vitro,

GBM,

U87MG

in-vitro,

GBM,

T98G

in-vitro,

GBM,

A172

"highlight2" >TumAuto↑, "highlight2" >ROS↑, "highlight2" >TumCD↑, "highlight2" >tumCV↓, "highlight2" >selectivity↑, "highlight2" >MMP↓, "highlight2" >eff↓, "highlight2" >MitoP↑,

5085-

SSE,

Intravenous Infusion of High Dose Selenite in End-Stage Cancer Patients: Analysis of Systemic Exposure to Selenite and Seleno-Metabolites

Review,

Var,

"highlight2" >toxicity↝, "highlight2" >Half-Life↝, "highlight2" >ROS↑, "highlight2" >Thiols↓, "highlight2" >NADPH↓, "highlight2" >toxicity↝, "highlight2" >other↝,

5084-

SSE,

GEM,

The Antitumor Activity of Sodium Selenite Alone and in Combination with Gemcitabine in Pancreatic Cancer: An In Vitro and In Vivo Study

in-vitro,

PC,

PANC1

5.6uM

vitro+vivo,

PC,

Panc02

 4.6 µM,

C57BL mice bearing a Pan02-generated tumor

"highlight2" >tumCV↓, "highlight2" >ChemoSen↑, "highlight2" >TumCG↓, "highlight2" >OS↑, "highlight2" >MMP↓, "highlight2" >AIF↑, "highlight2" >GSH↓, "highlight2" >Trx↓, "highlight2" >ROS↑, "highlight2" >AntiTum↑,

5083-

SSE,

Sodium Selenite as an Anticancer Agent

Review,

Var,

"highlight2" >AntiCan↑, "highlight2" >ROS↑,

5090-

SSE,

Sodium Selenite Induces Ferroptosis in Non-small Cell Lung Cancer A549 Cells Via Reactive Oxygen Species (ROS)/Glutathione (GSH)/Glutathione Peroxidase4 (GPx4) Axis

NA,

Lung,

A549

"highlight2" >TumCP↓, "highlight2" >ROS↑, "highlight2" >GSH↓, "highlight2" >MMP↓, "highlight2" >GPx4↓, "highlight2" >Iron↑,

5081-

SSE,

Application Notes and Protocols: Selenite as a Selenium Source in Cell Culture Media Supplementation

Review,

Var,

"highlight2" >Dose↝, "highlight2" >ROS↑, "highlight2" >Akt↓, "highlight2" >mTOR↓, "highlight2" >TumCCA↑, "highlight2" >Apoptosis↑,

5080-

SSE,

Sodium Selenite Regulates the Proliferation and Apoptosis of Gastric Cancer Cells by Suppressing the Expression of LncRNA HOXB-AS1

in-vitro,

GC,

HGC27

in-vitro,

GC,

NCI-N87

"highlight2" >AntiTum↑, "highlight2" >HOXB-AS1↓, "highlight2" >TumCP↓, "highlight2" >TumCI↓, "highlight2" >Apoptosis↑, "highlight2" >BAD↓, "highlight2" >Bcl-2↓, "highlight2" >cl‑Casp3↑, "highlight2" >MMP2↓, "highlight2" >E-cadherin↑, "highlight2" >N-cadherin↓, "highlight2" >ROS↑, "highlight2" >NF-kB↓,

5079-

SSE,

Rad,

The solvent and treatment regimen of sodium selenite cause its effects to vary on the radiation response of human bronchial cells from tumour and normal tissues

in-vitro,

Lung,

A549

in-vitro,

Nor,

BEAS-2B

"highlight2" >chemoP↑, "highlight2" >eff↝, "highlight2" >ROS↑, "highlight2" >MMP↓, "highlight2" >Cyt‑c↑, "highlight2" >TumCG↓, "highlight2" >RadioS↝, "highlight2" >other↝,

5078-

SSE,

Rad,

Results from a Phase 1 Study of Sodium Selenite in Combination with Palliative Radiation Therapy in Patients with Metastatic Cancer

Trial,

Pca,

33 mg dose level,

15 patients with metastatic cancer treated with selenite (5.5 to 49.5 mg) orally as a single dose 2 hours before each radiation therapy (RT) treatment.

"highlight2" >Half-Life↝, "highlight2" >OS↑, "highlight2" >Pain↓, "highlight2" >PSA↓, "highlight2" >GSH↓, "highlight2" >ROS↑, "highlight2" >selectivity↑, "highlight2" >TumCG↓, "highlight2" >AR↓, "highlight2" >Dose↑, "highlight2" >ChemoSen↑, "highlight2" >RadioS↑,

5077-

SSE,

Antitumor effects of sodium selenite on acute lymphocytic leukemia

in-vitro,

AML,

"highlight2" >TumCD↑, "highlight2" >Apoptosis↑,

5076-

SSE,

Sodium selenite inhibits the growth of cervical cancer cells through the PI3K/AKT pathway

in-vivo,

Cerv,

HeLa

BALB/c female nude mice, and then intraperitoneally injected with 3 mg/kg sodium selenite (SS) for 14 days

in-vivo,

Cerv,

SiHa

"highlight2" >TumCG↓, "highlight2" >toxicity↓, "highlight2" >tumCV↓, "highlight2" >Apoptosis↑, "highlight2" >p‑PI3K↓, "highlight2" >p‑Akt↓, "highlight2" >eff↑,

5075-

SSE,

Sodium selenite inhibits proliferation and metastasis through ROS‐mediated NF‐κB signaling in renal cell carcinoma

vitro+vivo,

RCC,

786-O

BALB/c athymic mice (6–8 weeks of age)

"highlight2" >TumCP↓, "highlight2" >TumCMig↓, "highlight2" >Apoptosis↑, "highlight2" >ROS↑, "highlight2" >NF-kB↓, "highlight2" >eff↓, "highlight2" >E-cadherin↑, "highlight2" >cl‑Casp3↑, "highlight2" >VEGF↓, "highlight2" >MMP9↓, "highlight2" >EMT↓, "highlight2" >MMP↓, "highlight2" >mtDam↑, "highlight2" >BAX↑, "highlight2" >Bcl-2↓,

5074-

SSE,

Application of Sodium Selenite in the Prevention and Treatment of Cancers

Review,

Var,

"highlight2" >Imm↑, "highlight2" >angioG↑, "highlight2" >DNArepair↑, "highlight2" >NK cell↑, "highlight2" >ROS↑, "highlight2" >AntiCan↑, "highlight2" >selectivity↑, "highlight2" >ER Stress↑, "highlight2" >TumAuto↑, "highlight2" >necrosis↑, "highlight2" >toxicity↝, "highlight2" >Dose↑,

5073-

SSE,

Pharmacokinetics and Toxicity of Sodium Selenite in the Treatment of Patients with Carcinoma in a Phase I Clinical Trial: The SECAR Study

Trial,

Var,

Patients received first line of chemotherapy following selenite treatment

"highlight2" >AntiTum↑, "highlight2" >ChemoSen↑, "highlight2" >Dose↑, "highlight2" >Half-Life↝, "highlight2" >toxicity↝, "highlight2" >toxicity↝,

5097-

SSE,

Examining xCT-mediated selenium uptake and selenoprotein production capacity in cells

in-vitro,

Var,

"highlight2" >other↝,

5112-

SSE,

https://pubmed.ncbi.nlm.nih.gov/19811770/

in-vitro,

Pca,

PC3

"highlight2" >VEGF↓, "highlight2" >IL6↓, "highlight2" >NF-kB↓, "highlight2" >p65↓,

5111-

SSE,

Sodium selenite induces apoptosis via ROS-mediated NF-κB signaling and activation of the Bax-caspase-9-caspase-3 axis in 4T1 cells

in-vitro,

BC,

4T1

"highlight2" >ROS↑, "highlight2" >NF-kB↓, "highlight2" >p65↓, "highlight2" >mtDam↑, "highlight2" >Casp9↑, "highlight2" >Casp3↑, "highlight2" >Apoptosis↑, "highlight2" >eff↓,

5110-

SSE,

Autophagy inhibition through PI3K/Akt increases apoptosis by sodium selenite in NB4 cells

in-vitro,

AML,

APL NB4

"highlight2" >Apoptosis↑, "highlight2" >selectivity↑, "highlight2" >TumAuto↓, "highlight2" >PI3K↓, "highlight2" >Akt↓,

5109-

SSE,

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

in-vitro,

CRC,

HCT116

"highlight2" >ROS↑, "highlight2" >DNAdam↓, "highlight2" >ATM↑, "highlight2" >eff↓, "highlight2" >TumCCA↑,

5108-

SSE,

Activation of p53 by sodium selenite switched human leukemia NB4 cells from autophagy to apoptosis

in-vitro,

AML,

U937

"highlight2" >p‑P53↑, "highlight2" >Beclin-1↓, "highlight2" >LC3I↓, "highlight2" >Apoptosis↑, "highlight2" >Casp↑,

5107-

SSE,

Involvement of p38 in signal switching from autophagy to apoptosis via the PERK/eIF2α/ATF4 axis in selenite-treated NB4 cells

vitro+vivo,

AML,

APL NB4

"highlight2" >PERK↑, "highlight2" >eIF2α↑, "highlight2" >ATF4↑, "highlight2" >Apoptosis↑, "highlight2" >AntiTum↑, "highlight2" >ER Stress↑, "highlight2" >p38↑,

5106-

SSE,

GSH,

Dual role of glutathione in selenite-induced oxidative stress and apoptosis in human hepatoma cells

in-vitro,

Liver,

HepG2

"highlight2" >ROS↑, "highlight2" >Apoptosis↑, "highlight2" >eff↑, "highlight2" >GSH↓,

5105-

SSE,

Sodium selenite induces apoptosis by generation of superoxide via the mitochondrial-dependent pathway in human prostate cancer cells

in-vitro,

Pca,

LNCaP

0, 0.5, 1.0, 1.5, 2.0, or 2.5 μM selenite for 5 days

"highlight2" >TumCD↑, "highlight2" >Apoptosis↑, "highlight2" >ROS↑, "highlight2" >eff↓, "highlight2" >MMP↓, "highlight2" >Cyt‑c↑, "highlight2" >Casp3↑, "highlight2" >Casp9↑, "highlight2" >ER Stress↑, "highlight2" >TumAuto↑, "highlight2" >necrosis↑, "highlight2" >chemoPv↑,

5089-

SSE,

Se,

Redox-mediated effects of selenium on apoptosis and cell cycle in the LNCaP human prostate cancer cell line

in-vitro,

Pca,

LNCaP

"highlight2" >ROS↑, "highlight2" >mtDam↑, "highlight2" >TumCD↑, "highlight2" >Apoptosis↑, "highlight2" >TumCCA↑, "highlight2" >Trx↓, "highlight2" >angioG↓, "highlight2" >GSH⇅, "highlight2" >NADPH↓, "highlight2" >GPx↑,

5096-

SSE,

Selenium Toxicity Accelerated by Out-of-Control Response of Nrf2-xCT Pathway

in-vitro,

BC,

MCF-7

"highlight2" >xCT↑, "highlight2" >ROS↑, "highlight2" >NRF2↑,

5095-

SSE,

Extracellular thiol-assisted selenium uptake dependent on the xc− cystine transporter explains the cancer-specific cytotoxicity of selenite

in-vitro,

Lung,

H157

"highlight2" >toxicity↝, "highlight2" >eff↓, "highlight2" >other↝, "highlight2" >ROS↑, "highlight2" >mtDam↑,

5094-

SSE,

Sodium Selenite Prevents Matrine-Induced Nephrotoxicity by Suppressing Ferroptosis via the GSH-GPX4 Antioxidant System

vitro+vivo,

Nor,

NRK52E

explored the involvement of ferroptosis in MT-induced kidney injury and evaluated the potential efficacy and underlying mechanism of sodium selenite (SS) in attenuating MT-induced nephrotoxicity.

"highlight2" >*GPx4↑, "highlight2" >*xCT↑, "highlight2" >*GSH↑, "highlight2" >*RenoP↑,

5093-

SSE,

Pharmacological mechanisms of the anticancer action of sodium selenite against peritoneal cancer in mice

in-vivo,

Var,

"highlight2" >AntiCan↑, "highlight2" >eff↑, "highlight2" >selectivity↑, "highlight2" >ROS↑, "highlight2" >Dose↝, "highlight2" >Trx↓, "highlight2" >GSH↓,

5092-

SSE,

Redox-Active Selenium Compounds—From Toxicity and Cell Death to Cancer Treatment

Review,

Var,

"highlight2" >*antiOx↑, "highlight2" >ROS↑, "highlight2" >GSH↓, "highlight2" >BioAv↓,

5091-

SSE,

Superoxide-mediated ferroptosis in human cancer cells induced by sodium selenite

in-vitro,

GBM,

U87MG

in-vitro,

Cerv,

HeLa

in-vitro,

BC,

MCF-7

in-vitro,

Pca,

PC3

in-vitro,

CRC,

HT-29

in-vitro,

Nor,

SVGp12

"highlight2" >Ferroptosis↑, "highlight2" >xCT↓, "highlight2" >GSH↓, "highlight2" >GPx4↓, "highlight2" >Iron↑, "highlight2" >lipid-P↑, "highlight2" >ROS↑, "highlight2" >eff↓, "highlight2" >TumCP↓, "highlight2" >TumCD↑,

4748-

SSE,

Chemo,

antiOx,

Efficacy and safety of intravenous administration of high-dose selenium for preventing chemotherapy-induced peripheral neuropathy in gastric cancer patients receiving adjuvant oxaliplatin and capecitabine after gastrectomy: a retrospective pilot study

Trial,

GC,

injection of selenium (2,000 μg/day) before chemotherapy

28 patients receiving adjuvant capecitabine plus oxaliplatin

"highlight2" >toxicity↓, "highlight2" >chemoP∅, "highlight2" >*neuroP↑, "highlight2" >*Dose↝,

1697-

SSE,

Calc,

Calcium intake may explain the reduction of colorectal cancer odds by dietary selenium - a case-control study in Poland

Human,

CRC,

"highlight2" >Risk↓, "highlight2" >Risk↓, "highlight2" >Dose∅, "highlight2" >AntiCan↑,

4753-

SSE,

Chemo,

Selenium and Lung Cancer: A Systematic Review and Meta Analysis

Review,

Lung,

"highlight2" >Risk⇅, "highlight2" >chemoP↑, "highlight2" >radioP↑,

4500-

SSE,

Dietary selenium affects host selenoproteome expression by influencing the gut microbiota

in-vivo,

Nor,

mice

"highlight2" >*GutMicro↑, "highlight2" >Risk↓, "highlight2" >*GPx↑,

4498-

SSE,

Selenium in Human Health and Gut Microflora: Bioavailability of Selenocompounds and Relationship With Diseases

Review,

Var,

Review,

AD,

Review,

IBD,

"highlight2" >*Imm↑, "highlight2" >*GutMicro↑, "highlight2" >*BioAv↑, "highlight2" >*Risk↓, "highlight2" >*Dose↝, "highlight2" >Risk↓, "highlight2" >*CRP↓, "highlight2" >*GPx↓, "highlight2" >*Inflam↓, "highlight2" >*selenoP↑, "highlight2" >*Dose↝, "highlight2" >*ROS↓, "highlight2" >*MDA↓, "highlight2" >*SOD↑, "highlight2" >*GPx↑, "highlight2" >*IL1↓, "highlight2" >*MCP1↓, "highlight2" >*IL6↓, "highlight2" >*TNF-α↓, "highlight2" >Risk↓, "highlight2" >*neuroP↑, "highlight2" >*memory↑,

4497-

SSE,

Selenium and inflammatory bowel disease

Review,

Var,

Review,

IBD,

"highlight2" >*GutMicro↑, "highlight2" >*selenoP↑, "highlight2" >*Inflam↓, "highlight2" >Risk↓, "highlight2" >*NF-kB↓, "highlight2" >*ROS↓,

4494-

SSE,

Advances in the study of selenium and human intestinal bacteria

Review,

IBD,

Review,

Var,

"highlight2" >*Risk↓, "highlight2" >OS↑, "highlight2" >*CRP↓, "highlight2" >*GPx↑, "highlight2" >*Inflam↓, "highlight2" >*ROS↓, "highlight2" >*GutMicro↑, "highlight2" >*selenoP↑, "highlight2" >*other↓,

4216-

SSE,

Selenium ameliorates mercuric chloride-induced brain damage through activating BDNF/TrKB/PI3K/AKT and inhibiting NF-κB signaling pathways

in-vitro,

NA,

Ninety male Hylan brown chickens

"highlight2" >*BDNF↑, "highlight2" >*TrkB↓, "highlight2" >*PI3K↑, "highlight2" >*Akt↑, "highlight2" >*neuroP↑,

1707-

SSE,

A Diet Lacking Selenium, but Not Zinc, Copper or Manganese, Induces Anticancer Activity in Mice with Metastatic Cancers

in-vivo,

Ovarian,

mice

in-vivo,

BC,

mice

"highlight2" >OS↓,

1706-

SSE,

Selenium in Prostate Cancer: Prevention, Progression, and Treatment

Review,

Pca,

"highlight2" >Risk∅, "highlight2" >ChemoSen↑, "highlight2" >Risk↓, "highlight2" >toxicity↝, "highlight2" >Risk↑, "highlight2" >eff↑, "highlight2" >*toxicity↑, "highlight2" >RadioS↑, "highlight2" >eff↓, "highlight2" >eff↑, "highlight2" >ChemoSen↑, "highlight2" >ChemoSideEff↓,

4610-

SSE,

Rad,

Protection during radiotherapy: selenium

Review,

Var,

"highlight2" >*radioP↑, "highlight2" >*antiOx↑, "highlight2" >*Inflam↓, "highlight2" >*DNAdam↓, "highlight2" >*lipid-P↓, "highlight2" >*selenoP↑, "highlight2" >*GPx1↑, "highlight2" >*BUN↓,

1688-

SSE,

Potential Role of Selenium in the Treatment of Cancer and Viral Infections

Review,

Var,

"highlight2" >IL2↑, "highlight2" >INF-γ↑, "highlight2" >Th1 response↑, "highlight2" >Th2↑, "highlight2" >Dose↑, "highlight2" >AntiCan∅, "highlight2" >Risk↑, "highlight2" >chemoP↑, "highlight2" >Hif1a↓, "highlight2" >VEGF↓, "highlight2" >selectivity↑, "highlight2" >*GADD45A↑, "highlight2" >NRF2↓, "highlight2" >*NRF2↑, "highlight2" >ChemoSen↑, "highlight2" >angioG↓, "highlight2" >PrxI↓, "highlight2" >ChemoSideEff↓, "highlight2" >eff↑,

1687-

SSE,

Selenium for preventing cancer

Analysis,

Var,

"highlight2" >eff∅, "highlight2" >AntiCan∅,

1062-

SSE,

Sodium Selenite Decreased HDAC Activity, Cell Proliferation and Induced Apoptosis in Three Human Glioblastoma Cells

in-vitro,

GBM,

LN229

in-vitro,

GBM,

T98G

in-vitro,

GBM,

U87MG

"highlight2" >HDAC↓, "highlight2" >TumCP↓, "highlight2" >TumCCA↑, "highlight2" >Apoptosis↑, "highlight2" >Casp3↝, "highlight2" >MMP2↓, "highlight2" >*BioAv↝,

1018-

SSE,

Selenite-induced autophagy antagonizes apoptosis in colorectal cancer cells in vitro and in vivo

vitro+vivo,

CRC,

HCT116

injected i.p. with sodium selenite (2 mg/kg/day

vitro+vivo,

CRC,

SW480

"highlight2" >TumAuto↑, "highlight2" >LC3s↑, "highlight2" >TumW↓, "highlight2" >Weight∅, "highlight2" >Beclin-1↑, "highlight2" >p62↓, "highlight2" >ROS↑,

1017-

SSE,

Selenite induces apoptosis in colorectal cancer cells via AKT-mediated inhibition of β-catenin survival axis

vitro+vivo,

CRC,

"highlight2" >Akt↓, "highlight2" >β-catenin/ZEB1↓, "highlight2" >cycD1/CCND1↓, "highlight2" >survivin↓, "highlight2" >Apoptosis↑, "highlight2" >ROS↑,

1003-

SSE,

Sodium selenite inhibits proliferation of lung cancer cells by inhibiting NF-κB nuclear translocation and down-regulating PDK1 expression which is a key enzyme in energy metabolism expression

vitro+vivo,

Lung,

"highlight2" >NF-kB↓, "highlight2" >PDK1↓, "highlight2" >p‑p65↑, "highlight2" >p‑IκB↑, "highlight2" >BAX↑, "highlight2" >lactateProd↓, "highlight2" >MMP↓, "highlight2" >Cyt‑c↑, "highlight2" >mitResp↑, "highlight2" >Apoptosis↑,

1002-

SSE,

Osi,

Adag,

Selenite as a dual apoptotic and ferroptotic agent synergizes with EGFR and KRAS inhibitors with epigenetic interference

in-vitro,

Lung,

H1975

7uM@72hr

in-vitro,

Lung,

H385

6uM@72hr

"highlight2" >Apoptosis↑, "highlight2" >Ferroptosis↑, "highlight2" >DNMT1↓, "highlight2" >TET1↑, "highlight2" >TumCCA↑, "highlight2" >cl‑PARP↑, "highlight2" >cl‑Casp3↑, "highlight2" >Cyt‑c↑, "highlight2" >BIM↑, "highlight2" >NOXA↑, "highlight2" >Apoptosis↑, "highlight2" >ROS↑, "highlight2" >ER Stress↑, "highlight2" >UPR↑,

4732-

SSE,

Selenium inhibits ferroptosis and ameliorates autistic-like behaviors of BTBR mice by regulating the Nrf2/GPx4 pathway

in-vivo,

Autism,

BTBR mice

"highlight2" >*Ferroptosis↓, "highlight2" >*NRF2↑, "highlight2" >*GPx4↑, "highlight2" >*other↝,

"highlight2" >RadioS∅, "highlight2" >radioP↑,

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 71

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

Sepsis↓, 1,
Total Targets: 159

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↓, 1, antiOx↑, 3, Catalase↑, 1, Ferroptosis↓, 2, GPx↓, 1, GPx↑, 5, GPx1↑, 1, GPx4↑, 3, GSH↑, 2, H2O2↓, 1, HO-1↑, 2, lipid-P↓, 1, MDA↓, 2, NRF2↑, 7, ROS↓, 8, selenoP↑, 8, SOD↑, 1, Trx↑, 1, xCT↑, 1,

Core Metabolism/Glycolysis ⓘ

BUN↓, 1,

Cell Death ⓘ

Akt↑, 1, Bcl-2↑, 1, Ferroptosis↓, 2,

Transcription & Epigenetics ⓘ

other↓, 3, other↑, 1, other↝, 3,

DNA Damage & Repair ⓘ

DNAdam↓, 2, GADD45A↑, 1,

Proliferation, Differentiation & Cell State ⓘ

PI3K↑, 1,

Immune & Inflammatory Signaling ⓘ

CRP↓, 2, IL1↓, 1, IL6↓, 2, Imm↑, 2, Inflam↓, 7, MCP1↓, 1, NF-kB↓, 2, NK cell↑, 1, TNF-α↓, 2,

Synaptic & Neurotransmission ⓘ

BDNF↑, 1, TrkB↓, 1,

Protein Aggregation ⓘ

NLRP3↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↑, 3, BioAv↝, 1, Dose↓, 1, Dose↝, 6, eff↑, 3, Half-Life↓, 1,

Clinical Biomarkers ⓘ

CRP↓, 2, GutMicro↑, 4, IL6↓, 2,

Functional Outcomes ⓘ

memory↑, 1, neuroP↑, 3, Pain↓, 1, QoL↑, 1, radioP↑, 2, RenoP↑, 1, Risk↓, 2, toxicity↓, 2, toxicity↑, 1, toxicity↝, 1, toxicity∅, 1,
Total Targets: 61

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#:148  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

Database Query Results : Selenite (Sodium), ,

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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