Oxidative Stress and Potential Antioxidant Therapies in Vitiligo: A Narrative Review

Abstract

Vitiligo is a chronic skin disorder characterised by the loss of melanocytes and subsequent skin depigmentation. Although many theories have been proposed in the literature, none alone explains the pathogenesis of vitiligo. Oxidative stress has been identified as a potential factor in the pathogenesis of vitiligo. A growing body of evidence suggests that antioxidant therapies may offer a promising approach to managing this condition. This review summarises the potential mechanisms of oxidative stress and the types of melanocyte death in vitiligo. We also provide a brief overview of the most commonly studied antioxidants. Melanocytes in vitiligo are thought to be damaged by an accumulation of reactive oxygen species to destroy the structural and functional integrity of their DNA, lipids, and proteins. Various causes, including exogenous and endogenous stress factors, an imbalance between prooxidants and antioxidants, disruption of antioxidant pathways, and gene polymorphisms, lead to the overproduction of reactive oxygen species. Although necroptosis, pyroptosis, ferroptosis, and oxeiptosis are newer types of cell death that may contribute to the pathophysiology of vitiligo, apoptosis remains the most studied cell death mechanism in vitiligo. According to studies, vitamin E helps to treat lipid peroxidation of the skin caused by psoralen ultra-violet A treatment. In addition, Polypodium leucotomos increased the efficacy of psoralen ultra-violet A or narrow-band ultraviolet B therapy. Our review provides valuable insights into the potential role of oxidative stress in pathogenesis and antioxidant-based supporting therapies in treating vitiligo, offering a promising avenue for further research and the development of effective treatment strategies.

Caffeic acid derivative WSY6 protects melanocytes from oxidative stress by reducing ROS production and MAPK activation

“…The skin is the largest organ in contact with the environment, and UV exposure makes melanocytes more likely to generate excess ROS when synthesizing melanin [ 1 , 4 , 5 , 29 , 30 ]. Previous studies have found that the entire epidermis of patients with vitiligo could be in a state of oxidative stress due to the accumulation of a large quantity of H 2 O 2 [ 31 ].…”

Phototherapy for vitiligo: A narrative review on the clinical and molecular aspects, and recent literature

“…Lastly, antioxidants might play a potential role in managing vitiligo, addressing oxidative stress, especially in conjunction with phototherapy; however, results from psoriasis studies also suggest that NBUVB might exert intrinsic antioxidant effects on its own 114,115 . In one study, the addition of alpha‐lipoic acid did not provide further benefit to NB‐UVB therapy in the treatment of stable NSV, whereas in another, pre‐treatment and concurrent supplementation with alpha‐lipoic acid before and during NB‐UVB significantly enhanced the clinical effectiveness of NBUVB and reduced vitiligo‐associated oxidative stress 116,117 .…”

Nghiên Cứu Nồng Độ Kẽm Huyết Thanh Trên Bệnh Nhân Bạch Biến Không Phân Đoạn

“…Nghiên cứu về giả thuyết tự miễn cho thấy vai trò của miễn dịch tế bào và cytokin viêm trong sự phát triển của bệnh bạch biến [5][6][7] . Giả thuyết stress oxy hóa cũng được ủng hộ bởi nghiên cứu ghi nhận nồng độ gốc oxy hóa cao bất thường trong mô thượng bì tổn thương bạch biến, dẫn đến suy chức năng và chết tế bào sắc tố 8,9 . Nguyên nhân của các tình trạng này đến nay chưa được biết rõ, và người ta đề xuất rằng kẽm -một chất vừa có vai trò điều hòa miễn dịch vừa có khả năng chống oxy hóa -bị thiếu hụt ở bệnh nhân bạch biến không phân đoạn.…”