Oxidative Stress in Vitiligo: Catalase Defects, H2O2 Accumulation, and Antioxidant Pathways

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Key Takeaways

  • Lesional epidermis often shows reduced catalase activity and increased H2O2, contributing to melanocyte stress and antigen exposure.
  • Systemic markers (e.g., MDA, 8-OHdG, GSH/GSSG imbalance) are elevated in subsets, supporting a body-wide oxidative tone in some patients.
  • NB-UVB can normalize redox signaling and melanogenic enzymes; pseudocatalase formulations and targeted antioxidants are under investigation.
  • Oxidative stress intersects with IFN-γ/CXCL10 immune pathways and may prime relapse at trauma-prone sites (Koebner).

Abstract

Multiple lines of evidence implicate oxidative stress in the initiation and propagation of vitiligo. Lesional skin frequently exhibits low catalase, accumulation of hydrogen peroxide, and alterations in tetrahydrobiopterin (BH4) metabolism. Systemic oxidative markers are elevated in subsets. We summarize core findings and discuss how NB-UVB, pseudocatalase preparations, and antioxidant strategies fit alongside immunomodulators.

Epidermal Evidence

Table 1. Redox abnormalities detected in lesional/perilesional skin.
Marker Typical finding Clinical note
Catalase activity Reduced vs. non-lesional controls Permits H2O2 build-up
H2O2 levels Elevated in stratum corneum Oxidizes melanogenic enzymes
BH4 / pterin cycle Dysregulated Impairs tyrosinase cofactor balance
Tyrosinase/catalase oxidation Post-translational modifications Functional inhibition

Systemic Biomarkers

Table 2. Selected circulating markers reported in cohorts.
Biomarker Pattern Comment
MDA (lipid peroxidation) ↑ in many cohorts Correlates with activity in some
8-OHdG (DNA oxidation) ↑ vs controls Oxidative DNA damage marker
GSH/GSSG ratio Shift to oxidized state Reflects antioxidant depletion
Total antioxidant capacity ↓ Heterogeneous across studies

Mechanisms Linking Oxidative Stress to Autoimmunity

  • Oxidative damage releases DAMPs and altered melanocyte antigens, facilitating IFN-γ/CXCL10 signaling and recruitment of CXCR3+ T cells.
  • Perifollicular niches with better antioxidant defenses explain early repigmentation “islands.”
  • Trauma/friction amplify local ROS → Koebnerization.

Therapeutic Implications

Table 3. Approaches that modulate redox milieu.
Strategy Rationale Clinical note
NB-UVB Normalizes cytokine/redox signaling; induces melanogenesis Backbone for widespread disease
Pseudocatalase (e.g., PC-KUS) Breaks down H2O2 Studied with UV/blue light activation
Targeted antioxidants Restore GSH; scavenge ROS Adjunctive; evidence mixed, dosing varies
JAK inhibitors Interrupt IFN-γ loop downstream of ROS priming See TRuE-V1/V2

Limitations

Assays and definitions are heterogeneous; many studies are small and cross-sectional. Direct causality and responder enrichment criteria for antioxidant-focused regimens remain open.

References

  1. Skin biochemistry studies reporting reduced catalase and increased H2O2 in lesional vitiligo.
  2. Cohort analyses of systemic oxidative markers (MDA, 8-OHdG, GSH/GSSG).
  3. Trials/series evaluating pseudocatalase and antioxidant adjuncts with phototherapy.
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