Description: <b>Selenium NanoParticles</b><br>
<pre>
| 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 |
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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. <br>
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<a href="https://nestronics.ca/dbx/tbResEdit.php?rid=4440">Se NPs might be hepatoprotective.</a><br>
<a href="https://nestronics.ca/dbx/tbResList.php?qv=149&tsv=1171&wNotes=on">(chemoprotective)</a>
<a href="https://nestronics.ca/dbx/tbResList.php?qv=149&tsv=1185&wNotes=on">(radioprotective)</a>
<a href="https://nestronics.ca/dbx/tbResList.php?qv=149&tsv=1107&wNotes=on">(radiosensitizer)</a><br>
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<pre>
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 dose
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Form of SeNPs matter:<br>
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.<br>
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.<br>
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.<br>
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"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."<br>
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SeNPs Cancer relevant pathways
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Rank</th>
<th>Pathway (direction)</th>
<th>Notes (key mechanistic readout)</th>
<th>Ref</th>
</tr>
<tr>
<td>1</td>
<td>Redox stress / ROS ↑</td>
<td>SeNPs commonly elevate intracellular ROS in cancer cells (often upstream of downstream apoptosis/autophagy signaling).</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC8582357/">(ref)</a></td>
</tr>
<tr>
<td>2</td>
<td>DNA damage / DDR ↑</td>
<td>ROS-linked DNA damage response reported in anti-angiogenic/cancer models (e.g., DNA damage as part of the cytotoxic cascade).</td>
<td><a href="https://pubmed.ncbi.nlm.nih.gov/26961468/">(ref)</a></td>
</tr>
<tr>
<td>3</td>
<td>PI3K → Akt → mTOR ↓</td>
<td>Frequently reported as inhibited (or functionally downshifted), aligning with reduced survival signaling and increased stress-death programs.</td>
<td><a href="https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2023.1116051/full">(ref)</a></td>
</tr>
<tr>
<td>4</td>
<td>Mitochondrial integrity (ΔΨm) ↓</td>
<td>Mitochondrial membrane potential loss is a recurring early event (mitochondria-centered cytotoxicity).</td>
<td><a href="https://royalsocietypublishing.org/doi/10.1098/rsos.180509">(ref)</a></td>
</tr>
<tr>
<td>5</td>
<td>Intrinsic apoptosis (caspase cascade) ↑</td>
<td>Activation of caspase-mediated apoptosis (e.g., caspase-3 activation) commonly follows mitochondrial disruption.</td>
<td><a href="https://royalsocietypublishing.org/doi/10.1098/rsos.180509">(ref)</a></td>
</tr>
<tr>
<td>6</td>
<td>Stress MAPK (p38) ↑</td>
<td>p38 signaling is reported as engaged in ROS-associated SeNP cytotoxicity programs (context: apoptosis signaling).</td>
<td><a href="https://pubmed.ncbi.nlm.nih.gov/30564384/">(ref)</a></td>
</tr>
<tr>
<td>7</td>
<td>p53 program ↑</td>
<td>p53 pathway activation/“reactivation” can be amplified in SeNP-based constructs (p53 target genes up; apoptosis up).</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC12615484/">(ref)</a></td>
</tr>
<tr>
<td>8</td>
<td>Autophagy regulation ↑ (often pro-death or dysregulated)</td>
<td>Functionalized SeNPs can drive autophagy as a major action mode in colorectal cancer models (often intertwined with cytotoxicity).</td>
<td><a href="https://pubmed.ncbi.nlm.nih.gov/30091749/">(ref)</a></td>
</tr>
<tr>
<td>9</td>
<td>Angiogenesis (VEGF → VEGFR2 → ERK/Akt) ↓</td>
<td>Anti-angiogenic SeNP designs suppress VEGF-driven signaling and tube formation in endothelial/tumor angiogenesis models.</td>
<td><a href="https://pubmed.ncbi.nlm.nih.gov/26961468/">(ref)</a></td>
</tr>
<tr>
<td>10</td>
<td>NF-κB signaling ↓</td>
<td>NF-κB activation markers (e.g., p-p65 / p-IκBα) can be reduced by decorated SeNPs in inflammatory signaling models relevant to tumor-promoting inflammation.</td>
<td><a href="https://link.springer.com/article/10.1186/s12951-017-0252-y">(ref)</a></td>
</tr>
<tr>
<td>11</td>
<td>Androgen receptor axis (AR transcriptional activity) ↓</td>
<td>Reported in prostate cancer context: AR downregulation/disruption via Akt/Mdm2/AR-linked apoptosis framework.</td>
<td><a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC3431821/">(ref)</a></td>
</tr>
<tr>
<td>12</td>
<td>Ferroptosis ↑ (Nrf2/HO-1/SLC7A11/GCLC/GPX4 ↓)</td>
<td>Some decorated SeNPs are explicitly reported to induce ferroptosis, including downregulation of System Xc−/GSH/GPX4-axis proteins and iron-homeostasis shifts.</td>
<td><a href="https://pubmed.ncbi.nlm.nih.gov/39701247/">(ref)</a></td>
</tr>
</table>