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전근 ( Gen Quan ),박미선 ( Mei Shan Piao ),최지영 ( Jee Young Choi ),전지선 ( Ji Sun Chun ),이지범 ( Jee Bum Lee ),이승철 ( Seung Chul Lee ) 대한피부과학회 2008 大韓皮膚科學會誌 Vol.46 No.6
Background: Although the pathogenesis of vitiligo isn`t fully understood, a recent study demonstrates that oxidative stress plays an important role to induce vitiligo. Peroxiredoxin (Prx) is a novel peroxidase family to remove hydrogen peroxide using thioredoxin system, which is consisted of thioredoxin, thioredoxin reductase, and NADPH. Objective: This study aimed to investigate the change of expression of Prx I to elucidate the role of oxidative stress in the pathogenesis of vitiligo. Methods: Sample specimens were obtained from the lesional skin of vitiligo patients, and non-depigmented skin was obtained from the perilesional area as control samples. The skin samples were immediately frozen using liquid nitrogen, and then section samples were prepared to perform immunohistochemical staining with antibodies for Prx I. Some of the skin biopsy samples were used for primary culture of keratinocytes. Protein extracts from the expanded keratinocytes were prepared for Western blot analysis of Prx I. Results: In vitiligo, the ubiquitous expression of Prx I in all layers of epidermis, which was also observed in the normal perilesional skin, was reduced in the depigmented lesion of vitiligo patients. The reduction of Prx I was remarkable from the lesions which were exposed to sunlight. Consistently, Prx I expression from the lesional keratinocytes were noticeably reduced in comparison with that from perilesional keratinocytes. Conclusion: Our results showing that Prx I is impaired in the epidermis of depigmented lesions of vitiligo patients suggest that oxidative stress is an important factor to induce vitiligo. (Korean J Dermatol 2008;46(6):736∼741)