Bor Boron
Features: micronutrient
Description: <b>Boron</b> is a trace mineral.<br>
Used in treating yeast infections, improving athletic performance, or preventing osteoporosis.<br>
<br>
Current research suggests that boric acid can modulate intercellular calcium levels—with potential implications for cancer therapy—by:<br>
-Altering calcium channel activity and calcium influx,<br>
-Modifying downstream calcium-dependent signaling, and<br>
-Inducing apoptotic pathways preferentially in cancer cells due to their altered calcium handling dynamics.<br>
Abnormal increases in [Ca²⁺]ᵢ can trigger mitochondrial dysfunction and activate calcium-dependent apoptotic pathways. Boric acid has been observed in some cell culture studies to induce apoptosis in cancer cells.<br>
In normal cells, modest changes in [Ca²⁺]ᵢ induced by boric acid may not reach a threshold that triggers apoptosis or other stress responses. This could lead to a relative sparing of normal cells compared to cancer cells.<br>
<br>
Pathways:<br>
1.Calcium Signaling Pathway<br>
In many cases, boron appears to normalize dysregulated calcium levels in cancer cells, often leading to an increase in calcium levels that can trigger calcium-dependent apoptotic pathways.
2.Apoptotic Pathways (Intrinsic and Extrinsic).<br>
Direction of Modulation:<br>
• Boron compounds may enhance the activation of apoptotic cascades.<br>
• Typically, an increase in intracellular calcium (as noted above) can further lead to mitochondrial dysfunction, cytochrome c release, and subsequent caspase activation, thereby promoting apoptosis.<br>
3.PI3K/AKT/mTOR Pathway<br>
• Some studies indicate that boron-containing compounds can inhibit this pathway.<br>
• Inhibition of PI3K/AKT/mTOR signaling reduces survival signals and can decrease cellular proliferation and growth in tumor cell.<br>
4.MAPK/ERK Pathway <br>
Boron may modulate the MAPK/ERK cascade by either dampening overactive mitogenic signals or altering the stress response.<br>
• This modulation can lead to reduced proliferation signals and may promote cell cycle arrest in cancer cells.<br>
5.NF-κB Signaling Pathway<br>
• Some reports indicate that boron compounds can suppress NF-κB activity.<br>
• This suppression might be achieved indirectly through modulation of upstream signals (such as changes in calcium or the cellular redox status) leading to decreased transcription of pro-survival and pro-inflammatory genes.<br>
6.Wnt/β-Catenin Pathway<br>
• Inhibition of Wnt/β-catenin signaling may interfere with proliferation and the maintenance of cancer stem cell populations.<br>
<br>
ROS:<br>
-ROS induction may be dose related.<br>
-Some studies report that when boron compounds are combined with other treatments (like chemotherapy or radiotherapy), there is a synergistic increase in ROS generation.<br>
Boron’s effects in a cancer context generally lean toward:<br>
• Normalizing dysregulated calcium signaling to push cells toward apoptotic death<br>
• Inhibiting pro-survival pathways such as <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC4712861/">PI3K/AKT/mTOR and NF-κB</a><br>
<br>
(1) is essential for the growth and maintenance of bone;<br>
(2) greatly improves wound healing;<br>
(3) beneficially impacts the body's use of estrogen, testosterone, and vitamin D;<br>
(4) boosts magnesium absorption;<br>
(5) reduces levels of inflammatory biomarkers, such as high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor α (TNF-α);<br>
(6) raises levels of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase;<br>
(7) protects against pesticide-induced oxidative stress and heavy-metal toxicity;<br>
(8) improves the brains electrical activity, cognitive performance, and short-term memory for elders;<br>
(9) influences the formation and activity of key biomolecules, such as S-adenosyl methionine (SAM-e) and nicotinamide adenine dinucleotide (NAD(+));<br>
(10) has demonstrated preventive and therapeutic effects in a number of cancers, such as prostate, cervical, and lung cancers, and multiple and non-Hodgkin's lymphoma; and<br>
(11) may help ameliorate the adverse effects of traditional chemotherapeutic agents.<br>
<br>
-Note <a href="tbResList.php?qv=46&tsv=1109&wNotes=on&exSp=open">half-life</a> 21 hrs average<br>
<a href="tbResList.php?qv=46&tsv=792&wNotes=on&exSp=open">BioAv</a> very high, 85-100%
<br>
Pathways:<br>
<!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑-->
- induce
<a href="tbResList.php?qv=46&tsv=275&wNotes=on">ROS</a> productionin cancer cells, while reducing ROS in normal cells.<br>
- ROS↑ related:
<a href="tbResList.php?qv=46&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm),
<a href="tbResList.php?qv=46&tsv=103&wNotes=on">ER Stress↑</a>,
<a href="tbResList.php?qv=46&tsv=459&wNotes=on">UPR↑</a>,
<a href="tbResList.php?qv=46&tsv=356&wNotes=on">GRP78↑</a>,
<a href="tbResList.php?qv=46&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>,(contrary)
<a href="tbResList.php?qv=46&tsv=77&wNotes=on">Cyt‑c↑</a>,
<a href="tbResList.php?qv=46&wNotes=on&word=Casp">Caspases↑</a>,
<a href="tbResList.php?qv=46&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>,
<a href="tbResList.php?qv=46&tsv=239&wNotes=on">cl-PARP↑</a>,(contrary)
<a href="tbResList.php?qv=46&wNotes=on&word=HSP">HSP↓</a>,
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=Prx">Prx</a>, --><!-- mitochondrial antioxidant enzyme-->
<br>
<!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, -->
- Debateable if Lowers AntiOxidant defense in Cancer Cells:
<a href="tbResList.php?qv=46&tsv=226&wNotes=on&word=NRF2">NRF2↓</a>(most contrary),
<!-- <a href="tbResList.php?qv=46&word=Trx&wNotes=on">TrxR↓**</a>, --><!-- major antioxidant system -->
<a href="tbResList.php?qv=46&tsv=298&wNotes=on&word=SOD">SOD↓</a>(some contrary),
<a href="tbResList.php?qv=46&tsv=137&wNotes=on&word=GSH↓">GSH↓</a>,
<a href="tbResList.php?qv=46&tsv=46&wNotes=on">Catalase↓</a>(some contrary),
<a href="tbResList.php?qv=46&tsv=597&wNotes=on">HO1↓</a>(contrary),
<a href="tbResList.php?qv=46&wNotes=on&word=GPx">GPx↓</a>(some contrary)
<br>
- Raises
<a href="tbResList.php?qv=46&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a>
defense in Normal Cells:
<a href="tbResList.php?qv=46&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>,
<a href="tbResList.php?qv=46&tsv=226&wNotes=on&word=NRF2">NRF2↑</a>,
<a href="tbResList.php?qv=46&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>,
<a href="tbResList.php?qv=46&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>,
<a href="tbResList.php?qv=46&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>,
<!-- genes involved in the oxidative stress-antioxidant defense system PRNP, NQO1, and GCLM -->
<br>
<!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, -->
- lowers
<a href="tbResList.php?qv=46&tsv=953&wNotes=on&word=Inflam">Inflammation</a> :
<a href="tbResList.php?qv=46&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>,
<a href="tbResList.php?qv=46&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=235&wNotes=on&word=p38↓">p38↓</a>, --> Pro-Inflammatory Cytokines :
<a href="tbResList.php?qv=46&tsv=908&wNotes=on&word=NLRP3↓">NLRP3↓</a>,
<a href="tbResList.php?qv=46&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>,
<a href="tbResList.php?qv=46&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>,
<a href="tbResList.php?qv=46&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=368&wNotes=on&word=IL8↓">IL-8↓</a> -->
<br>
<!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓
inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.-->
- inhibit Growth/Metastases :
<a href="tbResList.php?qv=46&tsv=604&wNotes=on">TumMeta↓</a>,
<a href="tbResList.php?qv=46&tsv=323&wNotes=on">TumCG↓</a>,
<a href="tbResList.php?qv=46&tsv=96&wNotes=on">EMT↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=204&wNotes=on">MMPs↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=201&wNotes=on">MMP2↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=203&wNotes=on">MMP9↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=308&wNotes=on">TIMP2</a>, -->
<a href="tbResList.php?qv=46&tsv=415&wNotes=on">IGF-1↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=428&wNotes=on">uPA↓</a>, -->
<a href="tbResList.php?qv=46&tsv=334&wNotes=on">VEGF↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=1284&wNotes=on">ROCK1↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=110&wNotes=on">FAK↓</a>, -->
<a href="tbResList.php?qv=46&tsv=273&wNotes=on">RhoA↓</a>,
<a href="tbResList.php?qv=46&tsv=214&wNotes=on">NF-κB↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=79&wNotes=on">CXCR4↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=1247&wNotes=on">SDF1↓</a>, -->
<a href="tbResList.php?qv=46&tsv=304&wNotes=on">TGF-β↓</a>,
<a href="tbResList.php?qv=46&tsv=719&wNotes=on">α-SMA↓</a>,
<a href="tbResList.php?qv=46&tsv=105&wNotes=on">ERK↓</a>
<!-- <a href="tbResList.php?qv=46&tsv=1178&wNotes=on">MARK4↓</a> --><!-- contributing to tumor growth, invasion, and metastasis-->
<br>
<!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, -->
- reactivate genes thereby inhibiting cancer cell growth :
<a href="tbResList.php?qv=46&tsv=140&wNotes=on">HDAC↓</a>,
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=DNMT">DNMTs↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=108&wNotes=on">EZH2↓</a>, -->
<a href="tbResList.php?qv=46&tsv=236&wNotes=on">P53↑</a>,
<a href="tbResList.php?qv=46&wNotes=on&word=HSP">HSP↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=506&wNotes=on">Sp proteins↓</a>, -->
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=TET">TET↑</a> -->
<br>
<!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ -->
- some indication of Cell cycle arrest :
<a href="tbResList.php?qv=46&tsv=322&wNotes=on">TumCCA↑</a>,
<a href="tbResList.php?qv=46&tsv=73&wNotes=on">cyclin D1↓</a>,
<a href="tbResList.php?qv=46&tsv=378&wNotes=on">cyclin E↓</a>,
<a href="tbResList.php?qv=46&tsv=467&wNotes=on">CDK2↓</a>,
<a href="tbResList.php?qv=46&tsv=894&wNotes=on">CDK4↓</a>,
<a href="tbResList.php?qv=46&tsv=895&wNotes=on">CDK6↓</a>,
<br>
<!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, -->
- inhibits Migration/Invasion :
<a href="tbResList.php?qv=46&tsv=326&wNotes=on">TumCMig↓</a>,
<a href="tbResList.php?qv=46&tsv=324&wNotes=on">TumCI↓</a>,
<a href="tbResList.php?qv=46&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>, <!-- encourages invasion, proliferation, EMT, and angiogenesis -->
<!-- <a href="tbResList.php?qv=46&tsv=110&wNotes=on">FAK↓</a>, -->
<a href="tbResList.php?qv=46&tsv=105&wNotes=on">ERK↓</a>,
<a href="tbResList.php?qv=46&tsv=96&wNotes=on">EMT↓</a>,
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=TOP">TOP1↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=657&wNotes=on">TET1</a>, -->
<br>
<!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS -->
- small indication of inhibiting
<a href="tbResList.php?qv=46&tsv=129&wNotes=on">glycolysis</a>
<!-- /<a href="tbResList.php?qv=46&tsv=947&wNotes=on">Warburg Effect</a> and
<a href="tbResList.php?qv=46&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> -->:
<a href="tbResList.php?qv=46&tsv=143&wNotes=on">HIF-1α↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=772&wNotes=on">PKM2↓</a>, -->
<a href="tbResList.php?qv=46&tsv=35&wNotes=on">cMyc↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=906&wNotes=on">LDH↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=175&wNotes=on&word=LDH">LDHA↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=773&wNotes=on">HK2↓</a>, -->
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=PFK">PFKs↓</a>, -->
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=PDK">PDKs↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=847&wNotes=on">ECAR↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=230&wNotes=on">OXPHOS↓</a>, -->
<a href="tbResList.php?qv=46&tsv=356&wNotes=on">GRP78↑</a>,
<a href="tbResList.php?qv=46&tsv=1278&wNotes=on">Glucose↓</a>,
<!--<a href="tbResList.php?qv=46&tsv=623&wNotes=on">GlucoseCon↓</a> -->
<br>
<!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)-->
- small indication of inhibiting
<a href="tbResList.php?qv=46&tsv=447&wNotes=on">angiogenesis↓</a> :
<a href="tbResList.php?qv=46&tsv=334&wNotes=on">VEGF↓</a>,
<a href="tbResList.php?qv=46&tsv=143&wNotes=on">HIF-1α↓</a>,
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=NOTCH">Notch↓</a>, -->
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=FGF">FGF↓</a>, -->
<!-- <a href="tbResList.php?qv=46&wNotes=on&word=PDGF">PDGF↓</a>, -->
<a href="tbResList.php?qv=46&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>,
<!--<a href="tbResList.php?qv=46&&wNotes=on&word=ITG">Integrins↓</a>, -->
<br>
<!-- CSCs : CSC↓, CK2↓, Hh↓, GLi↓, GLi1↓, -->
<!--
- inhibits Cancer Stem Cells :
<a href="tbResList.php?qv=46&tsv=795&wNotes=on">CSC↓</a>,
<a href="tbResList.php?qv=46&tsv=524&wNotes=on">CK2↓</a>,
<a href="tbResList.php?qv=46&tsv=141&wNotes=on">Hh↓</a>,
<a href="tbResList.php?qv=46&tsv=434&wNotes=on">GLi↓</a>,
<a href="tbResList.php?qv=46&tsv=124&wNotes=on">GLi1↓</a>,
<a href="tbResList.php?qv=46&tsv=677&wNotes=on">CD133↓</a>,
<a href="tbResList.php?qv=46&tsv=655&wNotes=on">CD24↓</a>,
<a href="tbResList.php?qv=46&tsv=342&wNotes=on">β-catenin↓</a>,
<a href="tbResList.php?qv=46&tsv=357&wNotes=on">n-myc↓</a>,
<a href="tbResList.php?qv=46&tsv=656&wNotes=on">sox2↓</a>,
<a href="tbResList.php?qv=46&wNotes=on&word=NOTCH">Notch2↓</a>,
<a href="tbResList.php?qv=46&tsv=1024&wNotes=on">nestin↓</a>,
<a href="tbResList.php?qv=46&tsv=508&wNotes=on">OCT4↓</a>,
<br> -->
<!-- OTHERS : -->
- Others: <a href="tbResList.php?qv=46&tsv=252&wNotes=on">PI3K↓</a>,
<a href="tbResList.php?qv=46&tsv=4&wNotes=on">AKT↓</a>,
<a href="tbResList.php?qv=46&wNotes=on&word=JAK">JAK↓</a>,
<a href="tbResList.php?qv=46&wNotes=on&word=STAT">STAT↓</a>,
<a href="tbResList.php?qv=46&tsv=377&wNotes=on">Wnt↓</a>,
<a href="tbResList.php?qv=46&tsv=342&wNotes=on">β-catenin↓</a>,
<a href="tbResList.php?qv=46&tsv=9&wNotes=on">AMPK</a>,
<!-- <a href="tbResList.php?qv=46&tsv=475&wNotes=on">α↓</a>, -->
<a href="tbResList.php?qv=46&tsv=105&wNotes=on">ERK↓</a>,
<!-- <a href="tbResList.php?qv=46&tsv=1014&wNotes=on">5↓</a>, -->
<!-- <a href="tbResList.php?qv=46&tsv=168&wNotes=on">JNK</a>, -->
- <a href="tbResList.php?qv=46&wNotes=on&word=SREBP">SREBP</a> (related to cholesterol).<br>
<!-- SYNERGIES : -->
- Synergies:
<a href="tbResList.php?qv=46&tsv=1106&wNotes=on">chemo-sensitization</a>,
<a href="tbResList.php?qv=46&tsv=1171&wNotes=on">chemoProtective</a>,
<a href="tbResList.php?qv=46&tsv=1107&wNotes=on">RadioSensitizer</a>,
<a href="tbResList.php?qv=46&tsv=1185&wNotes=on">RadioProtective</a>,
<a href="tbResList.php?qv=46&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>,
<a href="tbResList.php?qv=46&tsv=1105&wNotes=on">Neuroprotective</a>,
<a href="tbResList.php?qv=46&tsv=557&wNotes=on">Cognitive</a>,
<a href="tbResList.php?qv=46&tsv=1175&wNotes=on">Renoprotection</a>,
<a href="tbResList.php?qv=46&tsv=1179&wNotes=on">Hepatoprotective</a>,
<a href="tbResList.php?&qv=46&tsv=1188&wNotes=on">CardioProtective</a>,
<br>
<br>
<!-- SELECTIVE: -->
- Selectivity:
<a href="tbResList.php?qv=46&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a><br>
<br>
Boron Pathways for Cancer vs Normal cells
<table border="1" cellspacing="0" cellpadding="4">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer Cells</th>
<th>Normal Cells</th>
<th>Label</th>
<th>Primary Interpretation</th>
<th>Notes</th>
</tr>
<tr>
<td>1</td>
<td>Hormone / growth factor signaling (IGF-1, steroid modulation)</td>
<td>↓ growth-factor-driven proliferation</td>
<td>↔ optimized endocrine balance</td>
<td>Driver</td>
<td>Systemic growth signal modulation</td>
<td>Boron influences IGF-1, estrogen, and androgen signaling, indirectly reducing proliferative drive in hormone-responsive tumors</td>
</tr>
<tr>
<td>2</td>
<td>Inflammatory signaling (NF-κB / cytokines)</td>
<td>↓ pro-tumor inflammation</td>
<td>↓ inflammatory tone</td>
<td>Driver</td>
<td>Anti-inflammatory environment</td>
<td>Reduced chronic inflammation limits tumor-promoting microenvironmental signals</td>
</tr>
<tr>
<td>3</td>
<td>Cell membrane / signal transduction stability</td>
<td>↓ aberrant signaling responsiveness</td>
<td>↑ membrane and signaling stability</td>
<td>Secondary</td>
<td>Signal fidelity normalization</td>
<td>Boron supports membrane function and receptor signaling fidelity rather than directly inhibiting kinases</td>
</tr>
<tr>
<td>4</td>
<td>Mineral metabolism (Ca²⁺, Mg²⁺, vitamin D interaction)</td>
<td>↔ indirect growth restraint</td>
<td>↑ mineral homeostasis</td>
<td>Secondary</td>
<td>Metabolic support vs dysregulation buffering</td>
<td>Improved mineral balance supports normal cell resilience and systemic metabolic health</td>
</tr>
<tr>
<td>5</td>
<td>Reactive oxygen species (ROS)</td>
<td>↑ ROS (secondary, cancer-biased)</td>
<td>↔ or ↓ ROS (buffered)</td>
<td>Secondary</td>
<td>Metabolic-stress–linked oxidative pressure</td>
<td>ROS increase reflects impaired redox buffering and metabolic stress rather than direct redox chemistry</td>
</tr>
<tr>
<td>6</td>
<td>Glutathione (GSH) homeostasis</td>
<td>↓ GSH availability</td>
<td>↔ maintained</td>
<td>Secondary</td>
<td>Reduced antioxidant capacity</td>
<td>GSH depletion arises from impaired synthesis and NADPH support in cancer cells</td>
</tr>
<tr>
<td>7</td>
<td>Apoptosis</td>
<td>↔ minimal induction</td>
<td>↔ protected</td>
<td>Phenotypic</td>
<td>Non-cytotoxic profile</td>
<td>Boron does not act as a direct apoptotic trigger</td>
</tr>
</table>
<pre>
Distinct from compounds of main Redox Driver
| Compound | ROS ↑ mechanism | Category |
| ------------------- | --------------------------- | ------------------- |
| PEITC | Direct electrophilic stress | Redox driver |
| Selenium (selenite) | Redox cycling | Redox driver |
| Thymoquinone | Quinone cycling | Redox driver |
| **Boron** | Metabolic redox imbalance | **Secondary redox** |
</pre>