Antioxidant enzymes and lipid peroxidation at the tissue level in patients with stable and active vitiligo

Dammak, Ines; Boudaya, S.; Abdallah, Ferjani Ben; Turki, H.; Attia, Hamadi; Hentati, Basma

doi:10.1111/j.1365-4632.2009.03998.x

Cited by 71 publications

(63 citation statements)

References 18 publications

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“…Our results suggested that erythrocyte MDA levels were not altered in vitiligo patients regardless of disease activity. Previous studies have shown higher MDA levels in both serum and tissues in vitiligo patients compared to healthy controls 3,4,6,[8][9][10]15 .…”

Section: Discussionmentioning

confidence: 88%

“…The etiology of vitiligo remains unclear, but oxidative stress and the accumulation of free radicals have been proposed as important pathogenic mechanisms [3][4][5] . Increased malondialdehyde (MDA) levels are reported in the skin of patients with active vitiligo.…”

Section: Introductionmentioning

confidence: 99%

“…Increased malondialdehyde (MDA) levels are reported in the skin of patients with active vitiligo. Additionally, glutathione peroxidase (GPX) and superoxide dismutase (SOD) levels have been reported to be elevated in vitiligo patients 3,6 . The acquisition of tissue samples to test these levels is not easy, however.…”

Section: Introductionmentioning

confidence: 99%

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Erythrocyte Malondialdehyde and Glutathione Levels in Vitiligo Patients

et al. 2010

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Background:Vitiligo is an acquired and progressive hypomelanotic disease that manifests as circumscribed depigmented patches on the skin. Although the precise mechanism remains to be elucidated, an imbalance of the oxidant/antioxidant system has been proposed as an important etiologic mechanism. Objective: The objective of this study was to evaluate the oxidant/antioxidant status of vitiligo patients at the erythrocyte level. Methods: Fifty-three vitiligo patients and 65 phototype-, age-, and sex-matched healthy controls were included in this study. Blood samples were collected from all subjects, and all patients were instructed to answer a questionnaire. Results: Erythrocyte levels of malondialdehyde (MDA) and glutathione (GSH) were measured. All patients were told to answer a questionnaire regarding their habitual behavior, including frequency of smoking and type of diet. We observed significantly lower levels of GSH in vitiligo patients, but the levels of MDA did not differ between patients and controls. Vitiligo patients who smoked showed significantly lower GSH levels compared to non-smoking patients, but the levels of MDA were unchanged between the 2 groups. Conclusion: From our results, we conclude that reduced erythrocytic or systemic GSH levels constitute a distinctive feature in vitiligo patients regardless of disease activity.

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Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

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Erythrocyte Malondialdehyde and Glutathione Levels in Vitiligo Patients

et al. 2010

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“…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. [45] The ER is a sensor of cellular stress.…”

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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“…The biochemical theory ascribes the destruction of melanocytes to autocytotoxic metabolites, which derive from the synthesis of melanin. Several studies prove the presence of oxidative stress and the accumulation of free radicals in the epidermal layer of affected skin, and recently antioxidant enzymes and lipid peroxidation have been detected in the tissues of vitiligo patients [2,4]. Le Poole et al in 1993 worked out the ''convergence theory'', which suggests the synergistic role of all the above-mentioned factors and cells in the pathogenesis of vitiligo [9].…”

Section: Introductionmentioning

confidence: 99%

Dendritic cells: ultrastructural and immunophenotypical changes upon nb-UVB in vitiligo skin

et al. 2010

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The role of dendritic cells in vitiligo is still unclear. Few studies have provided contradictory results about their quantitative variation and no data exist concerning their immunophenotypical distribution in diseased skin. The purpose of our study was to analyze the presence, the distribution, the immunophenotypical markers and the effects of nb-UVB therapy on dendritic cells in nonlesional, perilesional, and lesional vitiligo skin. Punchbiopsies of 6 mm were taken from lesional, perilesional, and non-lesional skin of 12 patients affected by nonsegmental vitiligo, treated with nb-UVB. An immunohistochemical and an ultrastructural analysis were performed. Immunohistochemical and ultrastructural analysis showed both quantitative and qualitative modifications of Langerhans cells. Nb-UVB therapy, one of the most effective treatments for the disease, was able to reduce the Langerhans cells number and to redistribute main dendritic subsets. This study underlines the importance of dendritic cells, Langerhans cells in particular, in non-segmental vitiligo, in its pathogenesis and in its better therapeutical approach.

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Antioxidant enzymes and lipid peroxidation at the tissue level in patients with stable and active vitiligo

Abstract: Our study shows that oxidative stress is involved in the pathophysiology of both active and stable vitiligo, but an increased imbalance of antioxidants is observed in the tissues of patients with active vitiligo.

Cited by 71 publications

References 18 publications

Erythrocyte Malondialdehyde and Glutathione Levels in Vitiligo Patients

Erythrocyte Malondialdehyde and Glutathione Levels in Vitiligo Patients

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

Dendritic cells: ultrastructural and immunophenotypical changes upon nb-UVB in vitiligo skin

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