Health & Wellness, The Endocrine System
Antioxidants Produced by the Human Body
Our body produces antioxidants.
Below is a comprehensive map of the major endogenous antioxidants (produced by the human body), their biosynthesis pathways, primary roles, and links to health & wellbeing.
All are redox-active, recycled (not consumed like dietary vitamins), and tightly regulated by Nrf2-ARE signaling (the master antioxidant response pathway)
Below is a comprehensive map of the major endogenous antioxidants (produced by the human body), their biosynthesis pathways, primary roles, and links to health & wellbeing.
All are redox-active, recycled (not consumed like dietary vitamins), and tightly regulated by Nrf2-ARE signaling (the master antioxidant response pathway)
1. Core Enzymatic Antioxidants(Protein-based, transcriptionally induced via Nrf2)
|
Antioxidant
|
Biosynthesis / Cofactors
|
Primary Reaction
|
Health Impact
|
|---|---|---|---|
|
Superoxide Dismutase (SOD1/2/3)
|
• SOD1 (Cu/Zn, cytosol) • SOD2 (Mn, mitochondria) • SOD3 (Cu/Zn, extracellular)
|
2O₂⁻ + 2H⁺ → H₂O₂ + O₂
|
• ↓Mitochondrial ROS → prevents Parkinson’s, ALS • SOD2↑ in centenarians; SOD2⁻/⁻ mice die at ~3 weeks
|
|
Catalase (CAT)
|
Heme-containing, peroxisomes
|
2H₂O₂ → 2H₂O + O₂
|
• Detoxifies lipid peroxides; ↓ in Alzheimer’s plaques
|
|
Glutathione Peroxidase (GPx1–8)
|
Selenocysteine enzymes; Se required
|
2GSH + H₂O₂ → GSSG + 2H₂O
|
• GPx4: ferroptosis defense (lipid repair) • GPx1↓ in CVD, diabetes
|
|
Peroxiredoxins (PRDX1–6)
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Thioredoxin-dependent
|
ROOH + 2e⁻ → ROH + H₂O
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• PRDX2: neuronal H₂O₂ sensor; PRDX3: mitochondrial
|
|
Thioredoxin (Trx1/2)
|
NADPH → Trx reductase → Trx
|
Oxidized protein-SH → reduced
|
• ↑Cell survival in ischemia; ↓NF-κB inflammation
|
2. Non-Enzymatic Small-Molecule Antioxidants(Synthesized de novo or recycled)
|
Antioxidant
|
Synthesis Pathway
|
Redox Cycle
|
Health Role
|
|---|---|---|---|
|
Glutathione (GSH)
|
γ-Glu-Cys + Gly → GSH (GCL rate-limiting, Nrf2-induced)
|
GSH ⇌ GSSG (via GR + NADPH)
|
• Master antioxidant: 1–10 mM inity in cells • GSH/GSSG ratio = cellular redox poise • ↓GSH: aging, cancer, NASH, autism
|
|
Coenzyme Q10 (Ubiquinol, UQH₂)
|
Mevalonate → polyprenyl tail + benzoquinone (liver, mitochondria)
|
UQH₂ → UQ (Complex I/III) → UQH₂ (recycled)
|
• Electron carrier + lipid-soluble antioxidant • ↓UQH₂ in heart failure, statin myopathy
|
|
Uric Acid
|
Purine catabolism (xanthine oxidase)
|
Urate → allantoin (uricase absent in humans)
|
• Scavenges ONOO⁻, ·OH; 70% plasma antioxidant capacity • ↑Urate: gout; ↓urate: MS, Parkinson’s
|
|
Bilirubin
|
Heme → biliverdin → bilirubin (HO-1, Nrf2-induced)
|
Bilirubin ⇌ biliverdin (BVR)
|
• Potent peroxyl radical scavenger • Mild hyperbilirubinemia (Gilbert’s) = ↓CVD risk 50%
|
|
Melatonin (covered earlier)
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Tryptophan → serotonin → NAS → melatonin (pineal + extra-pineal)
|
Direct ROS scavenger; recycled via AFMK
|
See prior response
|
3. Secondary / Conditional Antioxidants (Induced under stress)
|
Molecule
|
Trigger
|
Role
|
|---|---|---|
|
Metallothionein (MT1/2)
|
Heavy metals, ROS, glucocorticoids
|
Binds Zn/Cu; scavenges ·OH; ↓ in aging brain
|
|
Ferritin
|
Iron + IRP-1/2
|
Sequesters Fe²⁺ → prevents Fenton reaction
|
|
Ceruloplasmin
|
Copper transport protein
|
Oxidizes Fe²⁺ → Fe³⁺ (safe storage)
|
|
Heme Oxygenase-1 (HO-1)
|
Nrf2 → Bach1 displacement
|
↑Bilirubin + CO (anti-apoptotic)
|
4. Redox Signaling & Wellbeing
These antioxidants are not just scavengers — they shape cellular decisions:
|
Function
|
Mechanism
|
Wellbeing Link
|
|---|---|---|
|
Redox Tone
|
GSH/GSSG, Trx-ox/red, Prx hyperoxidation
|
• Optimal ratio → growth, repair • Chronic oxidation → senescence
|
|
Nrf2-ARE Axis
|
ROS → KEAP1 dissociation → Nrf2 → 200+ genes
|
• Exercise, fasting, sauna ↑Nrf2 → longevity
|
|
Hormesis
|
Low-dose ROS → adaptive antioxidant response
|
• Explains benefits of HIIT, CR, sulforaphane
|
|
Circadian Redox
|
BMAL1/CLOCK ↑GPx, Prx; melatonin peaks at night
|
• Shift work → ↓GSH, ↑cancer/CVD
|
5. Clinical / Aging Correlations
|
Condition
|
Antioxidant Defect
|
Intervention
|
|---|---|---|
|
Neurodegeneration
|
↓SOD2, GPx4, GSH in substantia nigra
|
NAC, Se, α-lipoic acid
|
|
Cardiovascular
|
↓UQH₂, HO-1; ↑xanthine oxidase
|
CoQ10, allopurinol
|
|
Diabetes
|
↓GSH, ↑GSSG → insulin resistance
|
α-Lipoic acid (600 mg) ↑GSH
|
|
Cancer
|
Nrf2 hyperactivation in tumors (gain-of-function)
|
Avoid high-dose antiox in smokers
|
6. Boosting Endogenous Antioxidants (Evidence-Based)
|
Strategy
|
Target
|
Effect Size
|
|---|---|---|
|
Intermittent Fasting / CR
|
↑Nrf2, GSH, SOD2
|
+40% GSH in 24 h fast
|
|
Exercise (HIIT)
|
↑SOD2, GPx1 in muscle
|
+100% within 3 h
|
|
Sulforaphane (broccoli sprouts)
|
Nrf2 stabilizer
|
3–5× antioxidant enzymes
|
|
Cold/Warm Exposure
|
↑HO-1, bilirubin
|
+50% HO-1 in 2 h cold
|
|
Sleep & Melatonin
|
↑GSH recycling
|
+25% nocturnal GSH
|
|
Selenium (100–200 µg)
|
GPx4 synthesis
|
↑GPx activity 30%
|
Bottom Line
Your body operates a self-renewing antioxidant network, comprising GSH, SOD, GPx, CoQ10, bilirubin, and melatonin, all interconnected via Nrf2 and the circadian clock.
Wellbeing = maintaining youthful redox poise (not zero ROS).
Lifestyle > supplements: fasting, exercise, sleep, and plant Nrf2 activators amplify this system far beyond pills.
Wellbeing = maintaining youthful redox poise (not zero ROS).
Lifestyle > supplements: fasting, exercise, sleep, and plant Nrf2 activators amplify this system far beyond pills.
Source Grok X AI
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