Evaluation of Oxidative Stress in Red Blood Cells From Vitiligo Patients and Its Correlation With Disease Severity and Activity: A Cohort Case‐Control Study

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Authors: Yasser Salem N. Saleh, Ghada Farouk Mohammed, Maha Mohammed Anani, Altaf Bandy, Saleh Salem Bahaj, Radwa El‐Sayed Marie
Cited by: 1
References: 37

Abstract

ABSTRACT Background Exact pathogenesis of vitiligo is still ambiguous. Different theories explain the loss of melanocytes, such as autoimmune, biochemical, autocytotoxic, metabolic theories, or neural dysfunction theories. None of these theories have been proved yet. Objectives The goal of this investigation was to evaluate the burden of oxidative stress implicated in vitiligo pathogenesis. Methods We evaluated 30 patients with vitiligo and 30 healthy controls of a similar age and gender distribution. We measured catalase, superoxide dismutase (SOD), and glucose 6‐phosphate dehydrogenase (G6PD) activities in erythrocytes, as well as their plasma malondialdehyde (MDA) by spectrophotometry. Results SOD activity in red blood cells (RBCs) and serum MDA levels were significantly higher in vitiligo patients than controls ( p = 0.015, p = 0.013; respectively), positivity correlated with disease extent ( p = 0.03, p = 0.025; respectively), with the highest levels in universal vitiligo patients, and were significantly higher in disease activity ( p = 0.03). While catalase and G6PD activities were significantly lower in vitiligo patients than in controls ( p = 0.002, p = 0.010; respectively), negatively correlated with disease extent ( p = 0.04, p = 0.031; respectively), with the lowest levels in universal vitiligo, and were significantly lower in disease activity ( p = 0.03). Conclusion Our findings revealed that oxidative stress is probably implicated in vitiligo pathogenesis.

Fields of Study & Subjects

melanin and skin pigmentation Mast cells and histamine Retinoids in leukemia and cellular processes

Publication details

Journal / source
Health Science Reports
Publisher
Wiley
Volume
9
Issue
1
Pages
e71699–e71699
Publication date
1 January 2026
Language
EN