CUTANEOUS OXIDATIVE STRESS INDUCED BY POLLUTION (PARTICULATE MATTER) AND ITS AGGRAVATION BY ENVIRONMENTAL ULTRAVIOLET RADIATION (UV)

L. Marrot
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Abstract

Atmospheric pollution is a serious health concern and particulate matter (PM) from combustion is considered as particularly deleterious. In fact, ultrafine particles smaller than 100 nM in size contain toxic compounds such as poly aromatic hydrocarbons (PAH) adsorbed at their surface. Moreover, they can translocate from lung capillaries to blood circulation and be distributed in the whole body. Up to now, no precise estimation of pollutants in living skin is available, but plasma concentration can reach nanomolar range. Contamination of dermis and epidermis, either by penetration from skin surface or by systemic exposure, is highly probable since PAH can be found in cortex of human hair follicle. Some PAH are photo- reactive and phototoxic: sunlight and pollution might thus synergistically compromise skin health. After summing up current knowledge about dermatological damage induced by pollution, experimental data obtained in vitro using normal human keratinocytes or reconstructed epidermis will be presented. At very low concentrations (in the nanomolar range), some PAH such as benzopyrene or indenopyrene displayed a strong phototoxicity under exposure to daily UV (300-400 nm) and also to UVA1 (340-400 nm). Even when cytotoxicity was low, PAH- induced photo-oxidative stress could impair mitochondrial function (membrane polarization and ATP production) and impacted endogenous glutathione (GSH) homeostasis. Interestingly, among genes controlling GSH metabolism, SLC7A11 was particularly overexpressed (at gene and protein levels). This protein is an antiporter in charge of cystine supply. SLC7A11 upregulation suggests that regeneration of GSH might be of huge importance to ensure protection against “photo-pollution” stress. As proof, pretreatment of cells by buthionine sulfoximine BSO, an inhibitor of GSH biosynthesis, significantly increased PAH-induced phototoxicity. Our results highlight that pollutants could aggravate skin photodamage: specific photoprotection strategies for skin care in polluted area will be discussed.
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污染物(颗粒物)诱发的皮肤氧化应激及环境紫外线对皮肤氧化应激的加重
大气污染是一个严重的健康问题,燃烧产生的颗粒物(PM)被认为特别有害。事实上,尺寸小于100纳米的超细颗粒表面含有有毒化合物,如多环芳烃(PAH)。此外,它们可以从肺毛细血管转移到血液循环,分布在全身。到目前为止,活体皮肤中污染物的精确估计还没有实现,但血浆浓度可以达到纳摩尔范围。由于多环芳烃可以在人类毛囊皮层中发现,因此很可能通过皮肤表面渗透或全身暴露而污染真皮和表皮。一些多环芳烃具有光反应性和光毒性:阳光和污染可能因此协同损害皮肤健康。在总结了目前关于污染引起皮肤损伤的知识之后,我们将介绍利用正常人角质形成细胞或重建表皮在体外获得的实验数据。在非常低的浓度(在纳摩尔范围内),一些多环芳烃如苯并芘或茚并芘在每日暴露于紫外线(300-400 nm)和UVA1 (340-400 nm)下表现出很强的光毒性。即使在细胞毒性较低的情况下,多环芳烃诱导的光氧化应激也会损害线粒体功能(膜极化和ATP产生)并影响内源性谷胱甘肽(GSH)的稳态。有趣的是,在控制谷胱甘肽代谢的基因中,SLC7A11特别过度表达(在基因和蛋白质水平上)。这种蛋白质是负责胱氨酸供应的反向转运蛋白。SLC7A11的上调表明谷胱甘肽的再生可能对防止“光污染”胁迫具有重要意义。作为证据,用丁硫氨酸亚砜亚胺BSO(一种GSH生物合成抑制剂)预处理细胞,显著增加了pah诱导的光毒性。我们的研究结果强调污染物会加剧皮肤的光损伤,我们将讨论污染地区皮肤护理的具体光保护策略。
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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