The Role of Oxidants and Antioxidants in Generalized Vitiligo

Yıldırım, Mehmet; Baysal, Vahide; İnalöz, H. Serhat; Kesici, Demet; Delibaş, Namık

doi:10.1111/j.1346-8138.2003.tb00356.x

Cited by 85 publications

(87 citation statements)

References 17 publications

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“…Data on SOD levels are inconsistent, since both decreases 15 and increases [18][19][20]23 in SOD levels have been documented in the clinical course of vitiligo, with changes being linked to variations in the activity and duration of disease, different laboratory analyses 15 and different amounts of melanin as an antioxidant per se. 23 In the latter respect, comparison of active versus stabilized vitiligo revealed higher SOD activity in the active form: this was explained by the adaptation to increased oxidative stress in these patients. 18 In line with the findings of the present study, research conducted in patients with vitiligo in Turkey suggested that the simultaneous reduction in SOD levels and increase in MDA levels be a response to increased superoxide radicals.…”

Section: Discussionmentioning

confidence: 99%

Role of oxidative stress in the pathogenesis of vitiligo with special emphasis on the antioxidant action of narrowband ultraviolet B phototherapy

Karsli¹,

Akçalı

Özgöztaşı

et al. 2014

J Int Med Res

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Objectives: To evaluate the role of oxidative stress in the pathogenesis of vitiligo and the effect of narrowband (NB) ultraviolet (UV) B phototherapy on oxidative stress markers. Methods: Patients with vitiligo and healthy control subjects were included in the study. Patients in the vitiligo group were treated with an NB-UVB regimen (3 Â weekly for 6 months). Erythrocyte superoxide dismutase activity (SOD), erythrocyte malonyldialdehyde (MDA) and erythrocyte glutathione peroxidase activity (GSH-Px) levels were assessed in all participants at baseline, and after NB-UVB phototherapy in patients with vitiligo. Results: A total of 24 patients with vitiligo and 27 control subjects were included in the study. Before treatment, erythrocyte MDA levels were significantly higher, and SOD and GSH-Px levels were significantly lower, in patients with vitiligo compared with controls. NB-UVB phototherapy was associated with a significant reduction in MDA levels and a significant increase in GSH-Px levels, compared with baseline, in patients with vitiligo. Conclusion: NB-UVB phototherapy may relieve oxidative stress in patients with vitiligo by reversing the oxidant-antioxidant imbalance that is considered to play a role in the pathogenesis of this disease.

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Section: Discussionmentioning

confidence: 99%

Role of oxidative stress in the pathogenesis of vitiligo with special emphasis on the antioxidant action of narrowband ultraviolet B phototherapy

Karsli¹,

Akçalı

Özgöztaşı

et al. 2014

J Int Med Res

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“…[42] Oxidative stress and vitiligo A constant factor in many hypotheses regarding the pathobiology of vitiligo is the involvement of oxidative stress. Studies have suggested that individuals with vitiligo have a compromised antioxidant response, [43] with enzymes such as catalase and superoxide dismutase present at higher than expected levels in tissue from perilesional areas and in sera from patients with vitiligo. [44] Melanocytes in perilesional sites of vitiligo patients display hallmark dilation of the ER.…”

Section: Aetiologymentioning

confidence: 99%

Biology and genetics of oculocutaneous albinism and vitiligo – common pigmentation disorders in southern Africa

et al. 2013

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The primary pigment that determines human skin, hair and eye colour is melanin, which is synthesised by melanocytes. Melanin protects the skin from ultraviolet (UV) radiation and there is an inverse correlation between the degree of constitutive pigmentation and the risk of sun-induced skin cancers. Besides the life-threatening cancer risk, loss of pigmentation results in premature aging, compromised cutaneous immunity and significant emotional distress to affected individuals. [1][2][3] During embryonic development, melanocyte precursors that arise from the neural crest populate several areas including the interfollicular epidermis and hair follicle bulge in the skin; the uveal tract of the eye; and the stria vascularis, vestibular apparatus and endolymphatic sac of the ear. The development of melanocytes is tightly regulated at the genetic level by a number of genes that control proliferation, survival and migration of precursor cells to the various sites of the body and their differentiation into active melanocytes. A key regulator of this process is the microphthalmia transcription factor (MITF), which has been dubbed the 'master regulator' of the melanocyte, capable of modulating expression of several melanocytespecific proteins.[4] MITF mutations result in Waardenburg syndrome type II.[5] Once the melanocyte has differentiated, MITF regulates expression of genes in response to UV exposure, facilitating the tanning response.Melanocytes produce two forms of melanin, black-brown eumelanin and red-yellow pheomelanin. Skin and hair colour Corresponding author: P Manga (prashiela.manga@nyumc.org)Pigmentation disorders span the genetic spectrum from single-gene autosomal recessive disorders such as oculocutaneous albinism (OCA), the autosomal dominant disorder piebaldism to X-linked ocular albinism and multifactorial vitiligo. OCA connotes a group of disorders that result in hypopigmented skin due to decreased melanin production in melanocytes and loss of visual acuity. There are four non-syndromic forms, OCA1-4, which are classified based on the gene that is mutated (tyrosinase, OCA2, tyrosinase-related protein 1 and SLC45A2, respectively). Despite the fact that multiple genes account for the various forms of OCA, the phenotypes of all four forms result from disruption in the maturation and trafficking of the enzyme tyrosinase. OCA2 is the most prevalent autosomal recessive disorder among southern African blacks, affecting 1/3 900 individuals; while OCA3, although rare, is most prevalent in southern Africa. Another common pigmentation disorder in southern Africa is vitiligo, which affects 1 -2% of people worldwide. Vitiligo is a complex, acquired disorder in which melanocytes are destroyed due to an autoimmune response. The aetiology underlying this disorder is poorly understood, although recent genetic association studies have begun to shed light on the contributing factors. Pigmentation disorders have significant psychosocial implications and co-morbidities, yet therapies are still lacking. Recent progress in...

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“…Indicators of sustained oxidative stress are present in both serum and skin of individuals with vitiligo, [22][23][24] suggesting a reduced capacity to maintain intracellular redox balance. Melanocytes in vitiligo, subjected to additional oxidative stress, such as the influx of a chemotoxin, may undergo apoptosis more readily than normal melanocytes.…”

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confidence: 99%

A Role for Tyrosinase-Related Protein 1 in 4-tert-Butylphenol-Induced Toxicity in Melanocytes

Manga

Sheyn

Yang

et al. 2006

The American Journal of Pathology

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Vitiligo presents with depigmented cutaneous lesions following localized melanocyte death. Multiple factors contribute to cell death, including genetically determined susceptibility to trauma, and environmental factors, such as exposure to 4-tert-butylphenol (4-TBP). We demonstrate that 4-TBP induces oxidative stress that is more readily overcome by melanocytes from normally pigmented individuals than from two individuals with vitiligo. The antioxidant catalase selectively and significantly reduced death of melanocytes derived from two individuals with vitiligo, indicating a role for oxidative stress in vitiligo pathogenesis. In normal melanocytes, oxidative stress results in reduced expression of microphthalmia-associated transcription factor (MITF). Melanocyte-stimulating hormone-induced expression of MITF protein caused increased sensitivity to 4-TBP, whereas sensitivity of melanomas correlated with MITF expression. MITF stimulates melanin synthesis by up-regulating expression of melanogenic enzymes such as tyrosinase-related protein-1 (Tyrp1). Although melanin content per se did not affect sensitivity to 4-TBP, expression of Tyrp1 significantly increased sensitivity. Melanocytes and melanomas that express functional Tyrp1 were significantly more sensitive to 4-TBP than Tyrp1-null cells. Thus, normal melanocytes respond to 4-TBP by reducing expression of MITF and Tyrp1. We hypothesize that melanocytes in vitiligo demonstrate reduced ability to withstand oxidative stress due, partly, to a disruption in

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The Role of Oxidants and Antioxidants in Generalized Vitiligo

Cited by 85 publications

References 17 publications

Role of oxidative stress in the pathogenesis of vitiligo with special emphasis on the antioxidant action of narrowband ultraviolet B phototherapy

Role of oxidative stress in the pathogenesis of vitiligo with special emphasis on the antioxidant action of narrowband ultraviolet B phototherapy

Biology and genetics of oculocutaneous albinism and vitiligo – common pigmentation disorders in southern Africa

A Role for Tyrosinase-Related Protein 1 in 4-tert-Butylphenol-Induced Toxicity in Melanocytes

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