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      Assessment of Oxidative/Nitrosative Stress and Raftlin in Vitiligo

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          Abstract

          Background:

          Vitiligo is a chronic skin disease characterized by white macules on the skin due to loss of melanocytes. Although there are many theories about the etiopathogenesis of the disease, oxidative stress is identified as an important determinant in the etiology of vitiligo. In recent years, Raftlin has been shown to play a role in many inflammatory diseases.

          Aims:

          The aim of this study was to compare the patients with vitiligo and the control group to determine both oxidative/nitrosative stress markers and Raftlin levels.

          Materials and Methods:

          This study was designed prospectively between September 2017 and April 2018. Twenty-two patients diagnosed with vitiligo and 15 healthy people as the control group were included in the study. Blood samples collected to determine oxidative/nitrosative stress, the antioxidant enzyme, and Raftlin levels were sent to the biochemistry laboratory.

          Results:

          In patients with vitiligo, the activities of catalase, superoxide dismutase, glutathione peroxidase, and glutathione S transferase were significantly lower than in the control group ( P < 0.0001). In vitiligo patients, the levels of malondialdehyde, nitric oxide, nitrotyrosine (3-NTx), and Raftlin were significantly higher than in the control group ( P < 0.0001).

          Conclusions:

          The results of the study support that oxidative stress and nitrosative stress may play a role in the pathogenesis of vitiligo. In addition, the Raftlin level, a new biomarker of inflammatory diseases, was found high in patients with vitiligo.

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          Most cited references46

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          Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction.

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            Free radicals in the physiological control of cell function.

            At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, however, nitric oxide (NO), superoxide anion, and related reactive oxygen species (ROS) play an important role as regulatory mediators in signaling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and reestablish "redox homeostasis." Higher organisms, however, have evolved the use of NO and ROS also as signaling molecules for other physiological functions. These include regulation of vascular tone, monitoring of oxygen tension in the control of ventilation and erythropoietin production, and signal transduction from membrane receptors in various physiological processes. NO and ROS are typically generated in these cases by tightly regulated enzymes such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. In a given signaling protein, oxidative attack induces either a loss of function, a gain of function, or a switch to a different function. Excessive amounts of ROS may arise either from excessive stimulation of NAD(P)H oxidases or from less well-regulated sources such as the mitochondrial electron-transport chain. In mitochondria, ROS are generated as undesirable side products of the oxidative energy metabolism. An excessive and/or sustained increase in ROS production has been implicated in the pathogenesis of cancer, diabetes mellitus, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia/reperfusion injury, obstructive sleep apnea, and other diseases. In addition, free radicals have been implicated in the mechanism of senescence. That the process of aging may result, at least in part, from radical-mediated oxidative damage was proposed more than 40 years ago by Harman (J Gerontol 11: 298-300, 1956). There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.
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              Glutathione S-transferases. The first enzymatic step in mercapturic acid formation.

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                Author and article information

                Journal
                Indian J Dermatol
                Indian J Dermatol
                IJD
                Indian Journal of Dermatology
                Wolters Kluwer - Medknow (India )
                0019-5154
                1998-3611
                Sep-Oct 2022
                : 67
                : 5
                : 624
                Affiliations
                [1] From the Department of Dermatology, Faculty of Medicine, Kahramanmaras Sutcu Imam University, Kahramanmaras, Turkey
                [1 ] Department of Biochemistry, Faculty of Medicine, Kahramanmaras Sutcu Imam University, Kahramanmaras, Turkey
                Author notes
                Address for correspondence: Dr. Mehmet K Mulayim, Department of Dermatology, Sutcu Imam University Faculty of Medicine, Avsar Campus, 46100, Onikisubat, Kahramanmaras, Turkey. E-mail: kamilmulayim@ 123456gmail.com
                Article
                IJD-67-624d
                10.4103/ijd.ijd_917_20
                9971769
                36865862
                2b70db85-81ef-4241-87d3-f05fff667bc4
                Copyright: © 2022 Indian Journal of Dermatology

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                : October 2020
                : January 2022
                Categories
                Original Article

                Dermatology
                nitrosative stress,oxidative stress,pathogenesis,raftlin,vitiligo
                Dermatology
                nitrosative stress, oxidative stress, pathogenesis, raftlin, vitiligo

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