SUPEROXIDE DISMUTASE 1 AND 2 GENE POLYMORPHISM IN TURKISH VITILIGO PATIENTS
Tuna A1, Ozturk G1, Gerceker TB1, Karaca E2,*, Onay H2, Guvenc SM2, Cogulu O2
*Corresponding Author: Emin Karaca, M.D., Associacte Professor, Department of Dermatology and Venerology, Faculty of Medicine, Ege University, Kazım Dirik mah, Izmir, Turkey. Tel: +90-232-3903961-+90-532-2579285. Fax: +90-232- 3903971. E-mail: karacaemin@gmail.com
page: 67

INTRODUCTION

Vitiligo, characterized by milky-white patches on the skin, is an acquired disease of unknown etiology. Histologically speaking, it is caused by a loss of melanocytes [1]. Several theories have been proposed to explain the pathogenesis; these include the autoimmune, the neural and the theory of self-destruction. Most current studies have focused on the genetic etiology, with genes related to the autoimmunity, melanin, and the biological reply process to the oxidative stress, being the most thoroughly investigated [2-6]. With regard to the pathogenic role of oxidative stress in vitiligo, the previous studies were directed toward changes in antioxidant enzyme activity in the blood and tissue. Although some conflicting results were attained, all studies did point to an impact of oxidative stress on vitiligo [7-12]. Superoxide dismutase (SOD), one of the primary antioxidant enzymes, was previously studied in relation to vitiligo and to date, three isoforms of SOD have been identified in humans. They are coded by three different genes: copper-zinc SOD (CuZn-SOD), manganese SOD (Mn-SOD), and extracellular SOD. The diversity in their form stems from amino acid alignment, active metal zone and their intra cell location. Copper-zinc SOD, defined as SOD1, is a cytosolic enzyme, Mn-SOD, namely SOD2, exists in the mitochondria; while the expression of the SOD3 enzyme, is limited to only plasma, lymphoid tissue or cerebrospinal liquids [13,14]. Variations of SOD1 have previously been studied in relation to several clinical manifestations including amyo-trophic lateral sclerosis (ALS) and diabetes mellitus (DM) [15-17]. However, to the best of our knowledge, no studies considering associations between either gene polymorphism SOD1 35 A/C (rs2234694) or SOD2 A16V (C/T) (rs4880) and vitiligo is currently available in the literature. The aim of this study was to investigate the polymorphisms of the SOD1 and SOD2 and their impact on Turkish vitiligo patients.



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