Activation/deactivation of acetylcholinesterase by H2O2: more evidence for oxidative stress in vitiligo

Schallreuter, Karin U.; Elwary, Souna M.; Gibbons, Nicholas C. J.; Rokos, Hartmut; Wood, John M.

doi:10.1016/j.bbrc.2004.01.082

Cited by 165 publications

(109 citation statements)

References 26 publications

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“…Schallreuter et al considered the effect of H 2 O 2 on acetylcholinesterase (AchE). This enzyme was of interest because AchE levels were found to be lower in patients with vitiligo when compared with healthy controls, suggesting cholinergic involvement in the disease (Iyengar, 1989 as cited in Schallreuter et al, 2004). Skin biopsies from sun-unexposed areas from four healthy controls and four vitiligo patients.…”

Section: The Role Of Tetrahydrobiopterin Recycling and Other Indicatomentioning

confidence: 99%

“…Untreated depigmented skin showed very little catalase activity, and PC-KUS-treated skin showed significantly higher catalase expression throughout the epidermis compared to controls. Thus, H 2 O 2 levels were also found to have a concentration-dependent influence on AchE, i.e., low H 2 O 2 concentrations (approximately 10 -6 M or mol/L) activate AchE whereas high concentrations (10 -3 M or mol/L) deactivate AchE (Schallreuter et al, 2004). Butyrylcholinesterase (BchE) is an enzyme that mediates the hydrolysis of acetylcholine.…”

Section: The Role Of Tetrahydrobiopterin Recycling and Other Indicatomentioning

confidence: 99%

See 1 more Smart Citation

The Pathogenesis of Vitiligo

Dytoc¹,

Malhotr²

2011

Vitiligo - Management and Therapy

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Section: The Role Of Tetrahydrobiopterin Recycling and Other Indicatomentioning

confidence: 99%

Section: The Role Of Tetrahydrobiopterin Recycling and Other Indicatomentioning

confidence: 99%

The Pathogenesis of Vitiligo

Dytoc¹,

Malhotr²

2011

Vitiligo - Management and Therapy

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“…Accumulated oxidative stress leads to DNA damage, lipid and protein peroxidation and cell death (8,9). Hydrogen peroxide (H 2 O 2 )-mediated oxidation was reported to result in inhibition of tyrosinase (10) and the significant decrease in acetylcholine esterase (AChE) activity (11). A previous study showed that antioxidants may be resistant to cell death mediated by oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Quercetin attenuates the effects of H2O2 on endoplasmic reticulum morphology and tyrosinase export from the endoplasmic reticulum in melanocytes

Guan

Hong

et al. 2015

Molecular Medicine Reports

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Abstract. Swollen endoplasmic reticulum (ER) is commonly observed in the melanocytes of vitiligo patients; however, the cause and proteins involved in this remain to be elucidated. Oxidative stress has been reported to be involved in the pathogenesis of vitiligo and previous studies have demonstrated that hydrogen peroxide (H 2 O 2 ) induced melanocyte apoptosis, whereas quercetin exhibited cytoprotective activities against the effects of H 2 O 2 . The aim of the present study was to further investigate the role of H 2 O 2 in the ER of melanocytes as well as its role in the export of tyrosinase from ER; in addition, the present study aimed to determine the mechanism by which quercetin protects against the effects of H 2 O 2 . The results demonstrated that melanocyte cells treated with H 2 O 2 presented with swollen ER; however, a normal ER configuration was observed in untreated cells as well as quercetin/H 2 O 2 -treated cells. Furthermore, H 2 O 2 inhibited tyrosinase export from the ER and decreased expression levels of tyrosinase; however, quercetin was found to attenuate the effects induced by H 2 O 2 . In conclusion, the results of the present study confirmed the hypothesis that H 2 O 2 induced ER dilation and hindered functional tyrosinase export from the ER of melanocytes. It was also found that quercetin significantly weakened these effects mediated by H 2 O 2 , therefore it may have the potential for use in the treatment of vitiligo.

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“…13 In vitiligo, accumulation of toxic intermediates such as 6-and 7-BH4 and catecholamine, 14,15 concomitant with reduced levels and activity of catalase and several other antioxidant enzymes [16][17][18] have been demonstrated in patients' epidermis. Because of these intracellular metabolic disorder and compromised intrinsic antioxidant defenses, hydrogen peroxide (H 2 O 2 ) and other reactive oxygen species (ROS) accumulate in melanocytes, 19 which causes DNA damage and the peroxidation of lipid and protein, [20][21][22][23][24] thus disrupting the homeostasis of melanocytes. However, the specific molecular mechanism involved in oxidative stress-induced melanocyte death in vitiligo is not fully clarified, which impedes the discovery of novel drug target for the antioxidant therapy in vitiligo.…”

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confidence: 99%

Oxidative stress-induced overexpression of miR-25: the mechanism underlying the degeneration of melanocytes in vitiligo

et al. 2015

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Oxidative stress has a critical role in the pathogenesis of vitiligo. However, the specific molecular mechanism involved in oxidative stress-induced melanocyte death is not well characterized. Given the powerful role of microRNAs (miRNAs) in the regulation of cell survival as well as the fact that the generation of miRNAs can be affected by oxidative stress, we hypothesized that miRNAs may participate in vitiligo pathogenesis by modulating the expression of vital genes in melanocytes. In the present study, we initially found that miR-25 was increased in both serum and lesion samples from vitiligo patients, and its serum level was correlated with the activity of vitiligo. Moreover, restoration of miR-25 promoted the H 2 O 2 -induced melanocyte destruction and led to the dysfunction of melanocytes. Further experiments proved that MITF, a master regulator in melanocyte survival and function, accounted for the miR-25-caused damaging impact on melanocytes. Notably, other than the direct role on melanocytes, we observed that miR-25 inhibited the production and secretion of SCF and bFGF from keratinocytes, thus impairing their paracrine protective effect on the survival of melanocytes under oxidative stress. At last, we verified that oxidative stress could induce the overexpression of miR-25 in both melanocytes and keratinocytes possibly by demethylating the promoter region of miR-25. Taken together, our study demonstrates that oxidative stress-induced overexpression of miR-25 in vitiligo has a crucial role in promoting the degeneration of melanocytes by not only suppressing MITF in melanocytes but also impairing the paracrine protective effect of keratinocytes. Therefore, it is worthy to investigate the possibility of miR-25 as a potential drug target for anti-oxidative therapy in vitiligo. Vitiligo is a disfiguring dermatosis with an incidence rate of approximately 0.5-1.0% in the populations worldwide. 1 Characterized by patchy depigmentation of the skin, the disease can affect the patients' self-image, or even cause depression, thus substantially decreasing life quality among vitiligo patients. 2 Although several etiological theories, including genetic predisposition, 3-5 autoimmunity, 6,7 melanocytorrhagy 8,9 and toxic metabolites 10 have been proposed to participate in the pathogenesis of vitiligo, the exact mechanism of melanocyte degeneration in depigmented lesions still remains unclear.The generation of oxidative stress has long been demonstrated to have a crucial role in the onset and progression of vitiligo. 11,12 Owing to the pro-oxidant state generated during melanin synthesis, melanocytes are particularly vulnerable to oxidative stress. 13 In vitiligo, accumulation of toxic intermediates such as 6-and 7-BH4 and catecholamine, 14,15 concomitant with reduced levels and activity of catalase and several other antioxidant enzymes [16][17][18] have been demonstrated in patients' epidermis. Because of these intracellular metabolic disorder and compromised intrinsic antioxidant defenses, hydrogen peroxide (H 2 O ...

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Activation/deactivation of acetylcholinesterase by H2O2: more evidence for oxidative stress in vitiligo

Cited by 165 publications

References 26 publications

The Pathogenesis of Vitiligo

The Pathogenesis of Vitiligo

Quercetin attenuates the effects of H2O2 on endoplasmic reticulum morphology and tyrosinase export from the endoplasmic reticulum in melanocytes

Oxidative stress-induced overexpression of miR-25: the mechanism underlying the degeneration of melanocytes in vitiligo

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