DNA lesions triggered by visible light in skin cells: In the search for comprehensive sun protection

IF 3.261
Paulo Newton Tonolli , Orlando Chiarelli-Neto , Maurício S. Baptista
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引用次数: 0

Abstract

Skin cells present many endogenous photosensitizers (ePS) that interact with light, generating oxidizing species, causing molecular damage in proteins, lipids, and nucleic acids, and consequently triggering cellular and organelle malfunction. Several cell lines with terminal differentiation are susceptible to accumulating non-digestible pigments, such as lipofuscin or melanin-lipofuscin. Besides being hallmarks of aging, both pigments can work as photosensitizers, increasing and expanding the toxicity of sunlight to the range of visible light (VL, 400–700 nm). In here we review the literature to describe the mechanisms by which the photosensitized oxidation reactions induced by VL cause DNA damage. We aim to provide the mechanistic background needed to improve the current strategies of photoprotection.

皮肤细胞中可见光引发的DNA损伤:寻求全面的防晒
皮肤细胞存在许多内源性光敏剂(ePS),它们与光相互作用,产生氧化物质,导致蛋白质、脂质和核酸的分子损伤,从而引发细胞和细胞器功能障碍。一些终末分化的细胞系容易积累不可消化的色素,如脂褐素或黑色素-脂褐素。除了作为老化的标志,这两种色素都可以作为光敏剂,增加和扩大可见光范围内的毒性(VL, 400-700 nm)。本文综述了VL诱导的光敏氧化反应引起DNA损伤的机制。我们的目标是提供改进当前光保护策略所需的机制背景。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
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