Meta-analysis of the association between vitiligo and the level of superoxide dismutase or malondialdehyde

Shi, Meihui; Wu, Yan; Li, L.; Cai, Yunfei; Liu, M.; Gao, Xinghua; Chen, H.-D.

doi:10.1111/ced.12950

Cited by 23 publications

(19 citation statements)

References 18 publications

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“…However, ROS might not be scavenged by elevated CAT, SOD, and GPx instantly and effectively, yet ended up with a significant elevation. Meanwhile, the levels of SOD, CAT, and GPx activity are inconsistent with previous in vivo studies on vitiligo [34][35][36] , which indicates that the activity of antioxidation enzymes is changing dynamically at different stages of vitiligo. Thus, these results implied that ATG7dependent autophagy could influence the activity of antioxidation enzymes, but specific mechanisms of how autophagy regulates antioxidation enzymes need further investigation.…”

Section: Discussioncontrasting

confidence: 72%

Dysfunction of ATG7-dependent autophagy dysregulates the antioxidant response and contributes to oxidative stress-induced biological impairments in human epidermal melanocytes

Qiao

Xiao

et al. 2020

Cell Death Discov.

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Autophagy is a process involving the self-digestion of components that participates in anti-oxidative stress responses and protects cells against oxidative damage. However, the role of autophagy in the anti-oxidative stress responses of melanocytes remains unclear. To investigate the role of autophagy in human epidermal melanocytes, we knocked down and overexpressed ATG7, the critical gene of autophagy, in normal human epidermal melanocytes. We demonstrated that ATG7-dependent autophagy could affect melanin content of melanocytes by regulating melanogenesis. Moreover, suppression of ATG7-dependent autophagy inhibits proliferation and promotes oxidative stress-induced apoptosis of melanocytes, whereas enhancement of ATG7-dependent autophagy protects melanocytes from oxidative stress-induced apoptosis. Meanwhile, deficiency of ATG7-dependent autophagy results in premature senescence of melanocytes under oxidative stress. Notably, we verified that ATG7-dependent autophagy could alter oxidative stress homeostasis by regulating reactive oxygen species (ROS) production, nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway, and the activity of several antioxidant enzymes in melanocytes. In conclusion, our study suggested that ATG7-dependent autophagy is indispensable for redox homeostasis and the biological functions of melanocytes, such as melanogenesis, proliferation, apoptosis, and senescence, especially under oxidative stress.

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Section: Discussioncontrasting

confidence: 72%

Dysfunction of ATG7-dependent autophagy dysregulates the antioxidant response and contributes to oxidative stress-induced biological impairments in human epidermal melanocytes

Qiao

Xiao

et al. 2020

Cell Death Discov.

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“…SOD is a scavenger of endogenous ROS. A reduction of SOD activity not only results in insufficient clearance of oxygen radicals, but also induces the synthesis of MDA, resulting in cross-linking between molecules of the protein and in the molecule, and inducing apoptosis (33,34). GSH-Px is an important peroxide-degrading enzyme that protects the structure and function of cell membranes from peroxide injury (35).…”

Section: Discussionmentioning

confidence: 99%

PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

et al. 2020

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Recent growing evidence suggested that particulate matter 2.5 (PM2.5) has strong toxic effects on skin systems. However, the possible effects and the mechanisms of PM2.5 on vitiligo remain poorly understood. Therefore, the present study aimed to further investigate the effects and possible mechanisms of PM2.5 on vitiligo. Human keratinocytes (HaCaT cells) and human melanocytes (PIG1 cells and PIG3V cells) were exposed to PM2.5 (0-200 µg/ml) for 24 h. The cell viability of the three cell lines was measured by a Cell Counting Kit-8 assay. The secretions of stem cell factor (SCF) and basic fibroblast growth factor (bFGF) in HaCaT cells were evaluated by ELISA. The melanin contents, cellular tyrosinase activity, apoptosis, cell migration, malondialdehyde (MDA) contents, superoxide dismutase (SOD) levels, glutathione peroxidase (GSH-Px) levels and related protein expressions in PIG1 cells and PIG3V cells were evaluated by a NaOH assay, DOPA assay, Annexin V-FITC/Propidium Iodide staining, MDA assay, SOD assay, GSH-Px assay and western blotting, respectively. It was demonstrated that PM2.5 exposure inhibited cell viability of all three cell lines (HaCaT, PIG1 and PIG3V cells). PM2.5 exposure attenuated the secretions of SCF and bFGF in HaCaT cells. Moreover, PM2.5 exposure attenuated the activation of tyrosinase and melanogenesis, inhibited cell migration, and induced apoptosis and oxidative stress injury in PIG1 cells and PIG3V cells. In addition, PM2.5 exposure caused upregulated cytosolic cytochrome C and activated caspase-3 in PIG1 cells and PIG3V cells. Furthermore, PM2.5 exposure activated the nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 signaling pathway. The present results suggested that PM2.5 exposure could inhibit the secretions of SCF and bFGF in keratinocytes, and cause oxidative stress injury and melanin metabolic disorder in melanocytes. Therefore, PM2.5 could be a new risk factor for vitiligo. PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

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“…Though previous studies have shown an increased concentration of epidermal hydrogen peroxide, the recent findings seem contrary [ 44 ]. Reduced expression of catalase, and an enhanced expression of superoxide dismutase and consequent increased levels of malondialdehyde and DNA-peroxidation products have been described in many previous studies and established in a recent meta-analysis [ 45 ]. Another recent meta-analysis also shows that the levels of glutathione peroxidase are low in vitiligo [ 46 ].…”

Section: Stabilization Treatmentsmentioning

confidence: 99%

Clinical and Molecular Aspects of Vitiligo Treatments

Bishnoi

Parsad

2018

IJMS

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Vitiligo is an asymptomatic but cosmetically disfiguring disorder that results in the formation of depigmented patches on skin and/or mucosae. Vitiligo can be segmental or non-segmental depending upon the morphology of the clinical involvement. It can also be classified as progressing or stable based on the activity of the disease. Further, the extent of involvement can be limited (localized disease) or extensive (generalized disease). The treatment of vitiligo therefore depends on the clinical classification/characteristics of the disease and usually comprises of 2 strategies. The first involves arresting the progression of active disease (to provide stability) in order to limit the area involved by depigmentation. The second strategy aims at repigmentation of the depigmented area. It is also important to maintain the disease in a stable phase and to prevent relapse. Accordingly, a holistic treatment approach for vitiligo should be individualistic and should take care of all these considerations. In this review, we shall discuss the vitiligo treatments and their important clinical and molecular aspects.

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Meta-analysis of the association between vitiligo and the level of superoxide dismutase or malondialdehyde

Abstract: This meta-analysis showed a significant association between vitiligo and high levels of both SOD and MDA.

Cited by 23 publications

References 18 publications

Dysfunction of ATG7-dependent autophagy dysregulates the antioxidant response and contributes to oxidative stress-induced biological impairments in human epidermal melanocytes

Dysfunction of ATG7-dependent autophagy dysregulates the antioxidant response and contributes to oxidative stress-induced biological impairments in human epidermal melanocytes

PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

Clinical and Molecular Aspects of Vitiligo Treatments

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