Paulo Newton Tonolli , Orlando Chiarelli-Neto , Maurício S. Baptista
{"title":"DNA lesions triggered by visible light in skin cells: In the search for comprehensive sun protection","authors":"Paulo Newton Tonolli , Orlando Chiarelli-Neto , Maurício S. Baptista","doi":"10.1016/j.jpap.2023.100217","DOIUrl":null,"url":null,"abstract":"<div><p>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.</p></div>","PeriodicalId":375,"journal":{"name":"Journal of Photochemistry and Photobiology","volume":"18 ","pages":"Article 100217"},"PeriodicalIF":3.2610,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666469023000581/pdfft?md5=1e55efd127a6fe0916787d8c796651fc&pid=1-s2.0-S2666469023000581-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Photochemistry and Photobiology","FirstCategoryId":"2","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2666469023000581","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.