Department of Dermatology, Beaumont-Farmington Hills, Farmington Hills, Michigan.
Department of Dermatology, Henry Ford Hospital, Detroit, Michigan.
Photodermatol Photoimmunol Photomed. 2019 Nov;35(6):420-428. doi: 10.1111/phpp.12423. Epub 2018 Oct 15.
Oxidative stress is an integral element that influences a variety of biochemical reactions throughout the body and is known to play a notable role in melanogenesis. Exogenous triggers of oxidative stress, such as ultraviolet radiation (UVR) and visible light (VL), lead to pigment formation through somewhat different pathways, but both share a common endpoint-the potential to generate cosmetically undesirable hyperpigmentation. Though organic and inorganic sunscreens are available to protect against the UVR portion of the electromagnetic spectrum, coverage is lacking to protect against the VL spectrum. In this manuscript, we review the phases of tanning, pathways of melanogenesis triggered by UVR and VL, and the associated impact of oxidative stress. We also discuss the known intrinsic mechanisms and paracrine regulation of melanocytes that influence their response to UVR. Understanding these mechanisms and their role in UVR-induced hyperpigmentation should potentially lead to identification of useful targets that can be coupled with antioxidant therapy to alleviate this effect.
氧化应激是影响体内各种生化反应的一个重要因素,已知其在黑色素生成中起着重要作用。氧化应激的外源性触发因素,如紫外线辐射(UVR)和可见光(VL),通过不同的途径导致色素形成,但两者都有一个共同的终点——有可能产生美容上不希望的色素沉着过度。虽然有有机和无机防晒霜可用于防止电磁光谱的 UVR 部分,但缺乏对 VL 光谱的保护。在本文中,我们回顾了晒黑的各个阶段、UVR 和 VL 触发的黑色素生成途径,以及氧化应激的相关影响。我们还讨论了影响黑色素细胞对 UVR 反应的已知内在机制和旁分泌调节。了解这些机制及其在 UVR 诱导的色素沉着过度中的作用,有望确定有用的靶点,这些靶点可与抗氧化治疗相结合,以减轻这种影响。