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In contrast, when non-lesional skin is assessed, there are more oxidative pathway alterations in the skin of patients with vitiligo than of patients with other inflammatory skin diseases, suggesting that the depigmented areas are a phenotypically altered part of skin subjected to oxi-reducing imbalance.54 In addition to having a lower systemic antioxidant capacity (glutathione peroxidase reduction) when compared to individuals without vitiligo,55 there are differences in the serum levels of superoxide dismutase (SOD) and reduced glutathione (GSH) between patients with common and localized vitiligo, also assuming a difference in the systemic antioxidant status according to disease severity.56 Polymorphisms of FOXO3A, a gene with an important role in OS regulation, are also found in patients with active vitiligo.57 Treatment with narrowband UVB, in turn, is able to balance the redox status in patients with vitiligo, as demonstrated by the significant reduction in serum malondialdehyde (MDA) levels and an increase in glutathione peroxidase in patients treated by this phototherapy method.58 It is hypothesized that OS inflicts cell damage by inducing apoptosis in melanocytes, as well as other cell death mechanisms, such as ferroptosis and phagoptosis.52 Clinical and biochemical studies suggest that the overexpression of the TRPM2 gene (transient receptor potential cation channel subfamily M member 2) and the CGRP (calcitonin gene-related peptide) peptide are related to OS-sensitive calcium channels in perilesional melanocytes in vitiligo

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Burnichon N, Briere JJ, Libe R, Vescovo L, Rivière J, et al