Oxidative stress is implicated in the pathogenesis of lichen sclerosus

Abstract

This is the first study to demonstrate oxidative damage to lipids, DNA and proteins in LS, revealing a novel pathophysiological mechanism which may contribute to sclerosis, autoimmunity and carcinogenesis. Therapeutic strategies using antioxidants might be a useful new approach in the treatment of LS and could also help to prevent secondary malignancies.

Paediatric vulval lichen sclerosus

“…16 Another group of researchers compared vulval LS tissue from 16 patients with tissue from 16 vulval control samples and found a significant increase of lipid peroxidation products, particularly within epidermal basal cells, thus co-localizing with ECM-1. 17 The authors also demonstrated a significantly reduced expression of manganese superoxide dismutase, a mitochondrial enzyme that catalyses the reaction from superoxide anions to hydrogen peroxide. The enhanced oxidative stress caused by reduced enzyme expression could be a pathogenic factor in the autoimmune or neoplastic associations observed in some patients with LS.…”

Roles of serum uric acid, prolactin levels, and psychosocial factors in oral lichen planus

“…In LP, inflammatory cellular infiltrate, which mainly consists of CD4+ lymphocytes, is a well-known source of ROS (4). In high concentrations, ROS cause damage to endothelial cells and subsequently upregulate intercellular adhesion molecule 1 leading to the recruitment of T lymphocytes (5).…”

Formation of 8‐hydroxy‐2′‐deoxyguanosine in the DNA of cultured human keratinocytes by clinically used doses of narrowband and broadband ultraviolet B and psoralen plus ultraviolet A

“…(Cancer Sci 2006; 97: 99 -105) E ight-hydroxy-2′-deoxyguanosine (8-OH-dG), also known as 7,8-dihydro-8-oxo-deoxyguanosine (8-oxo-dG), (1) has been proposed as a key biomarker of oxidative DNA damage relevant to carcinogenesis (1,2) and pathogenesis of autoimmune disorders. (3,4) This DNA damage is induced by the reactions of reactive oxygen species (ROS), such as hydrogen peroxide (H 2 O 2 ), superoxide anions ( ), singlet oxygen and hydroxyl radicals (·OH).Human skin is constantly exposed to environmental stresses, and is vulnerable to the effects of ROS generated by exposure to ultraviolet (UV) radiation.(5) Yamamoto et al (6) reported that the formation of 8-OH-dG in DNA might be one of the mechanisms of daylight-induced mutagenesis. In fact, irradiation with a fluorescent sun lamp or with UVB does induce 8-OH-dG in the epidermis of hairless mice.…”

“…(Cancer Sci 2006; 97: 99 -105) E ight-hydroxy-2′-deoxyguanosine (8-OH-dG), also known as 7,8-dihydro-8-oxo-deoxyguanosine (8-oxo-dG), (1) has been proposed as a key biomarker of oxidative DNA damage relevant to carcinogenesis (1,2) and pathogenesis of autoimmune disorders. (3,4) This DNA damage is induced by the reactions of reactive oxygen species (ROS), such as hydrogen peroxide (H 2 O 2 ), superoxide anions ( ), singlet oxygen and hydroxyl radicals (·OH).…”

“…(3,4) This DNA damage is induced by the reactions of reactive oxygen species (ROS), such as hydrogen peroxide (H 2 O 2 ), superoxide anions ( ), singlet oxygen and hydroxyl radicals (·OH).…”