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含黄素氧化酶的激活是哺乳动物细胞中光诱导产生过氧化氢的基础。

Activation of flavin-containing oxidases underlies light-induced production of H2O2 in mammalian cells.

作者信息

Hockberger P E, Skimina T A, Centonze V E, Lavin C, Chu S, Dadras S, Reddy J K, White J G

机构信息

Department of Physiology, Northwestern University Medical School, 303 East Chicago Avenue, Chicago, IL 60611, USA.

出版信息

Proc Natl Acad Sci U S A. 1999 May 25;96(11):6255-60. doi: 10.1073/pnas.96.11.6255.

Abstract

Violet-blue light is toxic to mammalian cells, and this toxicity has been linked with cellular production of H2O2. In this report, we show that violet-blue light, as well as UVA, stimulated H2O2 production in cultured mouse, monkey, and human cells. We found that H2O2 originated in peroxisomes and mitochondria, and it was enhanced in cells overexpressing flavin-containing oxidases. These results support the hypothesis that photoreduction of flavoproteins underlies light-induced production of H2O2 in cells. Because H2O2 and its metabolite, hydroxyl radicals, can cause cellular damage, these reactive oxygen species may contribute to pathologies associated with exposure to UVA, violet, and blue light. They may also contribute to phototoxicity often encountered during light microscopy. Because multiphoton excitation imaging with 1,047-nm wavelength prevented light-induced H2O2 production in cells, possibly by minimizing photoreduction of flavoproteins, this technique may be useful for decreasing phototoxicity during fluorescence microscopy.

摘要

蓝紫光对哺乳动物细胞有毒性,这种毒性与细胞产生过氧化氢(H₂O₂)有关。在本报告中,我们表明蓝紫光以及紫外线A(UVA)可刺激培养的小鼠、猴子和人类细胞产生H₂O₂。我们发现H₂O₂起源于过氧化物酶体和线粒体,并且在过表达含黄素氧化酶的细胞中其产量增加。这些结果支持了黄素蛋白的光还原是细胞中光诱导产生H₂O₂的基础这一假说。由于H₂O₂及其代谢产物羟基自由基会导致细胞损伤,这些活性氧可能导致与暴露于UVA、紫光和蓝光相关的病理状况。它们也可能导致在光学显微镜检查过程中经常遇到的光毒性。由于波长为1047纳米的多光子激发成像可能通过最小化黄素蛋白的光还原而阻止细胞中光诱导的H₂O₂产生,该技术可能有助于降低荧光显微镜检查期间的光毒性。

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