Heck Diane E, Gerecke Donald R, Vetrano Anna M, Laskin Jeffrey D
Department of Pharmacology and Toxicology, Rutgers University, Piscataway, NJ 08854, USA.
Toxicol Appl Pharmacol. 2004 Mar 15;195(3):288-97. doi: 10.1016/j.taap.2003.09.028.
Ultraviolet light radiation in sunlight is known to cause major alterations in growth and differentiation patterns of exposed human tissues. The specific effects depend on the wavelengths and doses of the light, and the nature of the exposed tissue. Both growth inhibition and proliferation are observed, as well as inflammation and immune suppression. Whereas in the clinical setting, these responses may be beneficial, for example, in the treatment of psoriasis and atopic dermatitis, as an environmental toxicant, ultraviolet light can induce significant tissue damage. Thus, in the eye, ultraviolet light causes cataracts, while in the skin, it induces premature aging and the development of cancer. Although ultraviolet light can damage many tissue components including membrane phospholipids, proteins, and nucleic acids, it is now recognized that many of its cellular effects are due to alterations in growth factor- and cytokine-mediated signal transduction pathways leading to aberrant gene expression. It is generally thought that reactive oxygen intermediates are mediators of some of the damage induced by ultraviolet light. Generated when ultraviolet light is absorbed by endogenous photosensitizers in the presence of molecular oxygen, reactive oxygen intermediates and their metabolites induce damage by reacting with cellular electrophiles, some of which can directly initiate cell signaling processes. In an additional layer of complexity, ultraviolet light-damaged nucleic acids initiate signaling during the activation of repair processes. Thus, mechanisms by which solar ultraviolet radiation triggers cell signal transduction are multifactorial. The present review summarizes some of the mechanisms by which ultraviolet light alters signaling pathways as well as the genes important in the beneficial and toxic effects of ultraviolet light.
众所周知，阳光中的紫外线辐射会导致人体暴露组织的生长和分化模式发生重大改变。具体影响取决于光线的波长和剂量以及暴露组织的性质。生长抑制和增殖、炎症和免疫抑制都有观察到。在临床环境中，这些反应可能是有益的，例如在治疗牛皮癣和特应性皮炎时，但作为一种环境毒物，紫外线会导致显著的组织损伤。因此，在眼睛中，紫外线会导致白内障，而在皮肤中，它会导致过早衰老和癌症的发生。虽然紫外线会损害许多组织成分，包括膜磷脂、蛋白质和核酸，但现在人们认识到，它的许多细胞效应是由于生长因子和细胞因子介导的信号转导途径发生改变，导致异常的基因表达。一般认为，活性氧中间体是紫外线诱导的一些损伤的介质。当紫外线在分子氧存在下被内源性光敏剂吸收时产生，活性氧中间体及其代谢产物通过与细胞亲电试剂反应诱导损伤，其中一些亲电试剂可直接启动细胞信号传导过程。在另一个复杂层面上，紫外线损伤的核酸在修复过程激活期间引发信号传导。因此，太阳紫外线辐射触发细胞信号转导的机制是多因素的。本综述总结了紫外线改变信号通路的一些机制，以及在紫外线的有益和毒性作用中重要的基因。
