Abstract

Context:Premature canities etiopathogenesis is unclear, and approach to its therapy remains arbitrary. Reactive oxygen species generated during melanin biosynthesis in anagen hair bulb have been implicated in melanocyte apoptosis and hair graying. Extraneous factors, namely environmental pollution, stressful lifestyle, may compound the melanogenesis-induced endogenous oxidative stress.Aims:We aimed to investigate the role of systemic oxidative stress in causation of premature canities and its correlation with the severity of hair graying.Settings and Design:This was a tertiary care hospital-based cross-sectional study.Materials and Methods:Consecutive 50 patients with premature hair graying, aged <25 years, and 30 age and sex-matched healthy controls were recruited. Severity of premature canities was graded based on the total number of gray hair on the scalp. Redox status was evaluated in cases and controls, by malondialdehyde (MDA), reduced glutathione (rGSH), and superoxide dismutase (SOD) measurement in serum, by enzyme-linked immunosorbent assay.Results:Serum MDA concentration, an oxidative stress marker, was significantly higher (P < 0.01), while serum rGSH and SOD levels, both indicators of antioxidant potential, were significantly lower (P < 0.0001 and P < 0.01 respectively) in premature canities patients compared to controls. A novel observation was the significant correlation of serum MDA rise and serum rGSH decline with increasing severity of hair graying (P < 0.01 and P = 0.01, respectively).Conclusion:Systemic redox imbalance is present in premature canities patients, with the severity of hair graying varying in parallel to the degree of oxidative stress. Antioxidants supplementation is likely to yield therapeutic benefit in premature canities.

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