Increase in total blood antioxidant status and selenium levels in black patients with active vitiligo

Boisseau‐Garsaud, Anne‐Marie; Garsaud, Philippe; Lejoly‐Boisseau, Hélène; Robert, M.; Quist, D.; Arveiler, Benoı̂t

doi:10.1046/j.1365-4362.2002.01472.x

Cited by 34 publications

(42 citation statements)

References 25 publications

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“…Selenium is a cofactor for some isoforms of GSH-Px. Variable levels of GSH-Px and selenium have been found in tissue and blood of patients with active vitiligo [73,[83][84][85][126][127][128]. GST (glutathione transferase) is a superfamily of broadly expressed isoenzymes involved in defence against oxidative stress.…”

Section: Peroxinitritementioning

confidence: 99%

Vitiligo, reactive oxygen species and T-cells

2010

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The acquired depigmenting disorder of vitiligo affects an estimated 1% of the world population and constitutes one of the commonest dermatoses. Although essentially asymptomatic, the psychosocial impact of vitiligo can be severe. The cause of vitiligo remains enigmatic, hampering efforts at successful therapy. The underlying pathogenesis of the pigment loss has, however, been clarified to some extent in recent years, offering the prospect of effective treatment, accurate prognosis and rational preventative strategies. Vitiligo occurs when functioning melanocytes disappear from the epidermis. A single dominant pathway is unlikely to account for all cases of melanocyte loss in vitiligo; rather, it is the result of complex interactions of biochemical, environmental and immunological events, in a permissive genetic milieu. ROS (reactive oxygen species) and H2O2 in excess can damage biological processes, and this situation has been documented in active vitiligo skin. Tyrosinase activity is impaired by excess H2O2 through oxidation of methionine residues in this key melanogenic enzyme. Mechanisms for repairing this oxidant damage are also damaged by H2O2, compounding the effect. Numerous proteins and peptides, in addition to tyrosinase, are similarly affected. It is possible that oxidant stress is the principal cause of vitiligo. However, there is also ample evidence of immunological phenomena in vitiligo, particularly in established chronic and progressive disease. Both innate and adaptive arms of the immune system are involved, with a dominant role for T-cells. Sensitized CD8+ T-cells are targeted to melanocyte differentiation antigens and destroy melanocytes either as the primary event in vitiligo or as a secondary promotive consequence. There is speculation on the interplay, if any, between ROS and the immune system in the pathogenesis of vitiligo. The present review focuses on the scientific evidence linking alterations in ROS and/or T-cells to vitiligo.

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Section: Peroxinitritementioning

confidence: 99%

Vitiligo, reactive oxygen species and T-cells

2010

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“…Son zamanlarda yap›lan çal›flmalar vitiligoda hücresel oksidatif stresin etkilerine iflaret etmektedir [1][2][3][4] . Demir, hidroksil radikallerinin oluflumu üzerinden pigmentasyon bozukluklar›, inflamasyon ve kanserler dahil çeflitli deri hastal›klar›nda rol oynayan ve toksik etki gösterebilen bir elementtir.…”

Section: Giriflunclassified

“…Kan ferritin düzeyle-riyle ilgili tek çal›flma Boisseau-Garsaud ve ark. taraf›ndan kü-çük bir vitiligolu hasta gurubu üzerinde yap›lm›flt›r 3 . Yazarlar k›sa süre önce aktif vitiligo lezyonlar›n›n geliflti¤i 11 hasta ve yafl/cins uyumlu efl say›da kontrol bireyinde tam kan antioksidan durumu, serum selenyum, ferritin, transferrin, seruloplasmin, tokoferol ve retinol düzeylerini de¤erlendirmifllerdir.…”

Section: Tart›flmaunclassified

Serum Iron and Ferritin Levels in Patients with Vitiligo

Mansur¹,

Aydıngöz²,

Göktay³

et al. 2010

turkderm

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ÖzetAmaç: Son y›llarda vitiligoda oksidatif stresin rolü konusunda çok say›da araflt›rma yap›lmaktad›r. Demir ve ferritin inflamasyon ve oksidatif reaksiyonlarda önemli rollere sahiptir, ancak bugüne dek vitiligolu hastalardaki demir metabolizmas› konusunda çok az yay›n bulunmaktad›r. Bu çal›flmada lokalize ve jeneralize vitiligolu hastalar›n serum demir ve ferritin düzeylerinin bir kontrol gurubuyla karfl›laflt›rmal› olarak de¤erlendirilmesi amaçlanm›flt›r. Gereç ve Yöntem: Çal›flma guruplar› son 1 ayd›r sistemik tedavi veya fototerapi uygulanmayan vitiligolu 68 hasta ve yafl/cins uyumlu, tinea pedis, nevus ve keratozlar gibi vitiligo d›fl› deri hastal›¤› olan 72 kontrol bireyinden oluflmaktayd›. Her hasta ve kontrol bireyinden sözlü onay al›nd›ktan sonra kahvalt› öncesinde kan örnekleri al›nd›. Bulgular: Vitiligolu hastalarla kontrol bireyleri aras›nda serum demir ve ferritin düzeyleri aras›nda anlaml› farkl›l›k bulunamad› (p=0,478, p=0,307). Bu parametreler lokalize ve jeneralize vitiligolu hastalar aras›nda farkl›l›k göstermedi (p=0,054, p=0,867). Ayr›ca, serum demir ve ferritin düzeyleri ile hastal›k süreleri aras›nda anlaml› bir ba¤›nt› görülmedi (p=0,382, p=0,485). Sonuç: Sonuçlar›m›z serum demir ve ferritin düzeylerinin vitiligo ve kontrol bireyleri aras›nda benzer oldu¤unu göstermek-tedir. Demir ve ferritinin doku düzeylerinin belirlenece¤i yeni araflt›rmalar bu moleküllerin vitiligodaki olas› rollerine ›fl›k tutabilir. (Türkderm 2010; 44: 153-5) Anahtar Kelimeler: Demir, ferritin, hematolojik parametreler, oksidatif stres, vitiligo SummaryBackground and Design: In recent years, the role of oxidative stress in vitiligo has been widely investigated. Iron and ferritin have important roles in inflammation and oxidative reactions. However, up to date, there are very limited studies on iron metabolism in patients with vitiligo. In this study, we aimed to investigate serum iron and ferritin levels in patients with localized and generalized vitiligo in comparison with a control group. Material and Method: The study groups comprised 68 patients with vitiligo who did not receive systemic treatment or phototherapy in the preceding month, and 72 age-and sex-matched patients with skin disorders other than vitiligo including tinea pedis, melanocytic nevi, and keratoses. Blood samples for serum iron and ferritin levels were obtained before breakfast, after verbal informed consent. Results: No statistically significant differences were found between vitilligo patients and control population with regard to serum levels of iron and ferritin (p=0.478, p=0.307). Patients with localized and generalized vitiligo were also similar for these parameters (p=0.054, p=0.867). Moreover, serum levels of iron and ferritin did not show any significant correlation with disease duration (p=0.382, p=0.485). Conclusion: Our results showed that serum iron and ferritin levels were similar in patients with vitiligo and control subjects. Further studies determining the skin levels of iron and ferritin may elucidate the probable role of the...

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“…Whether the antioxidant defect is a general cellular feature in NSV or restricted to the epidermis has been investigated with variable results according to the type of blood cells studied (58,59). Unexpectedly, high serum selenium levels have been recorded in NSV patients (60,61). Occupational contact vitiligo because of phenolic derivatives has been studied as a model for NSV (62)(63)(64).…”

Section: Melanocyte Destructionmentioning

confidence: 99%

A Critical Appraisal of Vitiligo Etiologic Theories. Is Melanocyte Loss a Melanocytorrhagy?

Gauthier

andre

Taı̈eb

2003

Pigment Cell Research

264

211

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Common generalized vitiligo is an acquired depigmenting disorder characterized by a chronic and progressive loss of melanocytes from the epidermis and follicular reservoir. However, the mechanism of melanocyte disappearance has never been clearly understood, and the intervention of cellular and humoral autoimmune phenomena as primary events remains unproven. In this review, is discussed the data supporting the major theories of vitiligo, namely melanocyte destruction (autoimmune, neural and impaired redox status) and melanocyte inhibition or defective adhesion. Based on recent morphologic findings in vivo supporting a chronic detachment and transepidermal loss of melanocytes in common generalized vitiligo, a new theory is suggested proposing melanocytorrhagy as the primary defect underlying melanocyte loss, integrating most of the possible triggering/precipitating/ enhancing effects of other known factors.

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Increase in total blood antioxidant status and selenium levels in black patients with active vitiligo

Cited by 34 publications

References 25 publications

Vitiligo, reactive oxygen species and T-cells

Vitiligo, reactive oxygen species and T-cells

Serum Iron and Ferritin Levels in Patients with Vitiligo

A Critical Appraisal of Vitiligo Etiologic Theories. Is Melanocyte Loss a Melanocytorrhagy?

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