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Selenium NanoParticles| Category | Role in cancer | | -------------------------------- | ----------------------------------------------------------------------------------------------- | | Sodium Selenium (selenite) | Direct cytotoxic redox poison | | Selenium (organic / nutritional) | **Redox buffer & immune modulator** (generally *anti-therapy* when oxidative stress is desired) | | SeNPs | Tunable redox-signaling anticancer platform |The introduction of borneol led to a significant reduction in the size of selenium nanoparticles (SeNPs), as documented in the study (Prabhakaret et al., 2013). In the chemical synthesis of selenium nanoparticles, a precursor such as sodium selenite (Na₂SeO₃) is dissolved in water to form a homogenous solution. A reducing agent, like ascorbic acid or sodium borohydride (NaBH₄), is then added to the solution. The reducing agent donates electrons to the selenium ions (SeO32−SeO32), reducing them to elemental selenium (Se0Se^0). This reduction process leads to the nucleation of selenium atoms, which subsequently grow into nanoparticles through controlled aggregation. Se NPs might be hepatoprotective. (chemoprotective) (radioprotective) (radiosensitizer) Selenium nanoparticles (SeNPs) are a biocompatible, less-toxic, and more controllable form of selenium compared to inorganic salts (like sodium selenite). Major SeNPs hepatoprotective mechanisms Mechanism Description Key markers affected 1. Antioxidant activity SeNPs boost antioxidant enzyme ↓ ROS, ↓ MDA, ↑ GSH, ↑ GPx systems (GPx, SOD, CAT) and scavenge ROS directly. 2. Anti-inflammatory effect Downregulate NF-κB, TNF-α, ↓ TNF-α, ↓ IL-1β, ↓ IL-6 IL-6, and COX-2 pathways. 3. Anti-apoptotic action Balance between Bcl-2/Bax and reduce ↑ Bcl-2, ↓ Bax, ↓ Caspase-3 caspase-3 activation in hepatocytes. 4. Metal/toxin chelation SeNPs can bind or transform toxic ↓ liver metal accumulation metals (Cd²⁺, Hg²⁺, As³⁺) into less harmful complexes. 5. Mitochondrial protection Maintain membrane potential, Preserved ΔΨm, ↑ ATP prevent mitochondrial ROS burst, and ATP loss. 6. Regeneration support Stimulate hepatocyte proliferation ↑ PCNA, improved histology and repair via redox signaling and selenoproteins. Comparison: SeNPs vs. Sodium Selenite Property SeNPs Sodium Selenite Toxicity Low Moderate–high Bioavailability Controlled, often slow- Rapid, less controllable release ROS balance Adaptive, mild antioxidant Can flip to pro-oxidant easily Safety margin Wide Narrow Hepatoprotection Strong, sustained Protective at low dose, toxic at high doseForm of SeNPs matter: 1. Core composition / capping agent: SeNPs can be stabilized with polysaccharides, proteins, or small molecules. Some stabilizers may interact with cellular redox systems differently—e.g., a protein-capped SeNP may have slower release and less ROS generation, whereas a bare SeNP might induce stronger ROS in cancer cells. 2. Particle size: Smaller SeNPs (<50 nm) tend to generate more ROS and may enhance anticancer activity, but could theoretically interfere with ROS-dependent chemo if administered simultaneously. Larger SeNPs are slower-acting and may be safer alongside chemo. 3. Surface charge / coating: Positively charged or functionalized SeNPs can preferentially enter tumor cells, whereas neutral or negatively charged forms may distribute more evenly. This affects both selective cytotoxicity and interaction with normal cells. "30 mg of Na2SeO3.5H2O was added to 90 mL of Milli-Q water. Ascorbic acid (10 mL, 56.7 mM) was added dropwise to sodium selenite solution with vigorous stirring. 10 µL of polysorbate were added after each 2 ml of ascorbic acid. Selenium nanoparticles were formed after the addition of ascorbic acid. This can be visualized by a color change of the reactant solution from clear white to clear red. All solutions were made in a sterile environment by using a sterile cabinet and double distilled water." SeNPs Cancer relevant pathways
Selenium Nanoparticles (SeNPs) and Alzheimer’s Disease (AD)Overview: Selenium nanoparticles (SeNPs) are being investigated in Alzheimer’s disease primarily as a multifunctional neuroprotective nanoplatform rather than as a conventional nutrient supplement. In AD-oriented studies, SeNPs are used for one or more of the following: (1) direct inhibition of amyloid-β (Aβ) aggregation, (2) reduction of oxidative stress, (3) lowering of neuroinflammation, (4) improved blood-brain barrier (BBB) transport via targeting ligands, and/or (5) delivery or stabilization of partner compounds with poor brain availability. Current support is mainly from cell studies and rodent AD models, so the evidence is still experimental/preclinical, not established clinical therapy.
Mechanistic Summary
Overall Modulation Direction in AD
Evidence LevelPreclinical. The AD literature for SeNPs is mainly cell culture and rodent-model work. Formulation-specific effects are important; benefits shown for one coated or ligand-targeted SeNP system should not automatically be generalized to all selenium nanoparticles or to ordinary selenium supplementation. Notes / Interpretation
SeNP-Associated Products / Components Used in AD-Oriented Nanoformulations
Bottom LineFor AD, selenium nanoparticles appear most relevant as a multi-target anti-amyloid / antioxidant nanocarrier platform. Their strongest support is for reducing Aβ aggregation and oxidative-neuroinflammatory injury while improving delivery of partner neuroprotective compounds. At present, this is a research-stage strategy, not a validated clinical AD treatment. |
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| Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer. ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations. However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS. -mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related) "Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways." "During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity." "ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−". "Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules." Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea. Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells." Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers. -It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis. Note: Products that may raise ROS can be found using this database, by: Filtering on the target of ROS, and selecting the Effect Direction of ↑ Targets to raise ROS (to kill cancer cells): • NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS. -Targeting NOX enzymes can increase ROS levels and induce cancer cell death. -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS • Mitochondrial complex I: Inhibiting can increase ROS production • P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes) • Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels • Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels • Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels • SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels • PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels • HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS • Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production. -Inhibiting fatty acid oxidation can increase ROS levels • ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels • Autophagy: process by which cells recycle damaged organelles and proteins. -Inhibiting autophagy can increase ROS levels and induce cancer cell death. • KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes. -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death. • DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels • PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels • SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels • AMPK activation: regulates energy metabolism and can increase ROS levels when activated. • mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels • HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited. • Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels • Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS. -Increasing lipid peroxidation can increase ROS levels • Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation. -Increasing ferroptosis can increase ROS levels • Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability. -Opening the mPTP can increase ROS levels • BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited. • Caspase-independent cell death: a form of cell death that is regulated by ROS. -Increasing caspase-independent cell death can increase ROS levels • DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS • Epigenetic regulation: process by which gene expression is regulated. -Increasing epigenetic regulation can increase ROS levels -PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS) ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx) -HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more -Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research -Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2) Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference -generated from AI and Cancer database ROS rating: +++ strong | ++ moderate | + weak | ± mixed | 0 none NRF2: ↓ suppressed | ↑ activated | ± mixed | 0 none Conditions: [D] dose [Fe] metal [M] metabolic [O₂] oxygen [L] light [F] formulation [T] tumor-type [C] combination
|
| 6043- | CGA, | SeNPs, | Enhanced Effect of Combining Chlorogenic Acid on Selenium Nanoparticles in Inhibiting Amyloid β Aggregation and Reactive Oxygen Species Formation In Vitro |
| - | in-vitro, | AD, | NA |
| 6049- | EGCG, | SeNPs, | Epigallocatechin-3-gallate (EGCG)-stabilized selenium nanoparticles coated with Tet-1 peptide to reduce amyloid-β aggregation and cytotoxicity |
| - | Study, | AD, | PC12 |
| 6056- | RES, | SeNPs, | A comparative study of resveratrol and resveratrol-functional selenium nanoparticles: Inhibiting amyloid β aggregation and reactive oxygen species formation properties |
| - | Study, | AD, | NA |
| 6054- | RES, | SeNPs, | Oral Administration of Resveratrol-Selenium-Peptide Nanocomposites Alleviates Alzheimer's Disease-like Pathogenesis by Inhibiting Aβ Aggregation and Regulating Gut Microbiota |
| - | in-vivo, | AD, | NA |
| 6051- | RES, | SeNPs, | Chit, | Resveratrol-loaded selenium/chitosan nano-flowers alleviate glucolipid metabolism disorder-associated cognitive impairment in Alzheimer's disease |
| - | in-vivo, | AD, | NA |
| 4714- | Se, | SSE, | SeNPs, | Selenium in cancer management: exploring the therapeutic potential |
| - | Review, | Var, | NA |
| 4735- | SeNPs, | Selenium triggers Nrf2-AMPK crosstalk to alleviate cadmium-induced autophagy in rabbit cerebrum |
| - | in-vivo, | Nor, | NA |
| 4721- | SeNPs, | A review on selenium nanoparticles and their biomedical applications |
| - | Review, | AD, | NA | - | Review, | Diabetic, | NA | - | Review, | Arthritis, | NA |
| 4612- | SeNPs, | Rad, | Histopathological Evaluation of Radioprotective Effects: Selenium Nanoparticles Protect Lung Tissue from Radiation Damage |
| - | in-vivo, | Nor, | NA |
| - | in-vitro, | Nor, | NA |
| 6057- | SeNPs, | Dual-functional selenium nanoparticles bind to and inhibit amyloid β fiber formation in Alzheimer's disease |
| - | in-vitro, | AD, | PC12 |
| 6060- | SeNPs, | Multifunctional Selenium Quantum Dots for the Treatment of Alzheimer's Disease by Reducing Aβ-Neurotoxicity and Oxidative Stress and Alleviate Neuroinflammation |
| - | Study, | AD, | NA |
| 6063- | SeNPs, | Large Amino Acid Mimicking Selenium-Doped Carbon Quantum Dots for Multi-Target Therapy of Alzheimer's Disease |
| - | in-vivo, | AD, | NA |
| 6064- | SeNPs, | Multifunctional selenium-doped carbon dots for modulating Alzheimer's disease related toxic ions, inhibiting amyloid aggregation and scavenging reactive oxygen species |
| - | NA, | AD, | NA |
| 4450- | SeNPs, | Functionalized selenium nanoparticles with nephroprotective activity, the important roles of ROS-mediated signaling pathways |
| - | in-vitro, | Kidney, | NA |
| 4457- | SeNPs, | Selenium nanoparticles: a review on synthesis and biomedical applications |
| - | Review, | Var, | NA | - | NA, | Diabetic, | NA |
| 4452- | SeNPs, | Chit, | Antioxidant capacities of the selenium nanoparticles stabilized by chitosan |
| - | in-vitro, | Nor, | 3T3 |
| 4446- | SeNPs, | Antioxidant and Hepatoprotective Effects of Moringa oleifera-mediated Selenium Nanoparticles in Diabetic Rats. |
| - | in-vivo, | Diabetic, | NA |
| 4445- | SeNPs, | DFE, | A comparative study on the hepatoprotective effect of selenium-nanoparticles and dates flesh extract on carbon tetrachloride induced liver damage in albino rats |
| - | in-vivo, | LiverDam, | NA |
| 4444- | SeNPs, | Antioxidant and Hepatoprotective Efficiency of Selenium Nanoparticles Against Acetaminophen-Induced Hepatic Damage |
| - | in-vivo, | LiverDam, | NA |
| 4441- | SeNPs, | The Role of Selenium Nanoparticles in the Treatment of Liver Pathologies of Various Natures |
| - | Review, | Nor, | NA |
| 4440- | SeNPs, | AgNPs, | Selenium, silver, and gold nanoparticles: Emerging strategies for hepatic oxidative stress and inflammation reduction |
| - | Review, | NA, | NA |
| 4602- | SeNPs, | AgNPs, | GoldNP, | Advances in nephroprotection: the therapeutic role of selenium, silver, and gold nanoparticles in renal health |
| - | NA, | Nor, | NA |
| 4503- | SeNPs, | Prophylactic supplementation with biogenic selenium nanoparticles mitigated intestinal barrier oxidative damage through suppressing epithelial-immune crosstalk with gut-on-a-chip |
| - | in-vitro, | Nor, | NA |
| 4491- | SeNPs, | Chit, | VitC, | Synthesis of a Bioactive Composition of Chitosan–Selenium Nanoparticles |
| - | Study, | NA, | NA |
| 4472- | SeNPs, | Therapeutic potential of selenium nanoparticles |
| - | Review, | Var, | NA |
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#:391 Target#:275 State#:% Dir#:1
wNotes=0 sortOrder:rid,rpid