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紫外线诱导的活性氧在光致癌作用和光老化中的作用

UV-induced reactive oxygen species in photocarcinogenesis and photoaging.

作者信息

Scharffetter-Kochanek K, Wlaschek M, Brenneisen P, Schauen M, Blaudschun R, Wenk J

机构信息

Department of Dermatology, University of Cologne, Germany.

出版信息

Biol Chem. 1997 Nov;378(11):1247-57.

PMID:9426184
Abstract

The increase in UV irradiation on earth due to the stratospheric ozone depletion represents a major environmental threat to the skin increasing its risk of photooxidative damage by UV-induced reactive oxygen species (ROS). Increased ROS load has been implicated in several pathological states including photoaging and photocarcinogenesis of the skin. Large efforts have been made to better define the involvement of distinct ROS in photocarcinogenesis and photoaging. Both pathological processes share common features; however, they reveal unique molecular characteristics which finally determine the fate of the cell and its host. As well as causing permanent genetic changes involving protooncogenes and tumor suppressor genes, ROS activate cytoplasmic signal transduction pathways that are related to growth differentiation, senescence, transformation and tissue degradation. This review focuses on the role of UV-induced ROS in the photodamage of the skin resulting in biochemical and clinical characteristics of photocarcinogenesis and photoaging. A decrease in the ROS load by efficient sunscreens and/or otherwise protective agents may represent a promising strategy to prevent or at least minimize ROS induced cutaneous pathological states.

摘要

由于平流层臭氧消耗导致地球上紫外线辐射增加,这对皮肤构成了重大环境威胁,增加了皮肤因紫外线诱导的活性氧(ROS)而发生光氧化损伤的风险。ROS负荷增加与多种病理状态有关,包括皮肤的光老化和光致癌作用。人们已经做出了巨大努力来更好地确定不同ROS在光致癌作用和光老化中的作用。这两种病理过程有共同特征;然而,它们也揭示了独特的分子特征,这些特征最终决定了细胞及其宿主的命运。除了导致涉及原癌基因和肿瘤抑制基因的永久性基因变化外,ROS还激活与生长分化、衰老、转化和组织降解相关的细胞质信号转导途径。本综述重点关注紫外线诱导的ROS在皮肤光损伤中的作用,以及光致癌作用和光老化的生化和临床特征。通过有效的防晒霜和/或其他保护剂降低ROS负荷可能是预防或至少最小化ROS诱导的皮肤病理状态的一种有前景的策略。

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