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向秀丽隐杆线虫投喂活性氧(ROS)生成剂会导致其小分子热休克蛋白 HSP-16.2 和应激反应表达增加。

Feeding a ROS-generator to Caenorhabditis elegans leads to increased expression of small heat shock protein HSP-16.2 and hormesis.

机构信息

Department of Food and Nutrition, Molecular Nutrition Unit, Technical University of Munich, Am Forum 5, 85350, Freising, Germany.

出版信息

Genes Nutr. 2009 Mar;4(1):59-67. doi: 10.1007/s12263-009-0113-x. Epub 2009 Feb 28.

DOI:10.1007/s12263-009-0113-x
PMID:19252938
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2654055/
Abstract

Reactive oxygen species (ROS) are thought to be a driving force in the aging process. In transgenic Caenorhabditis elegans expressing green fluorescent protein (GFP) under control of the hsp-16.2 promoter (CL2070) 100 muM of the ROS-generator juglone induced GFP-expression. This was associated with translocation of DAF-16 to the nucleus as visualized in a transgenic strain expressing a DAF-16::GFP fusion protein (TJ356) and with increased cellular levels of reduced glutathione. RNA-interference for DAF-16 in CL2070 blocked the juglone-induced HSP-16.2 expression and the increase in glutathione levels. Higher concentrations of juglone did not further increase the adaptive responses but caused premature death, indicating hormetic adaptations unless the stressor exceeds the intrinsic protective capacity. The addition of the ROS-scavenger ascorbic acid finally blocked lifespan reductions and all of the adaptations to juglone stressing that ROS are indeed the molecular species that require protective response.

摘要

活性氧(ROS)被认为是衰老过程的驱动力。在转 Caenorhabditis elegans 中,绿色荧光蛋白(GFP)在 hsp-16.2 启动子(CL2070)的控制下表达,100μM 的 ROS 发生器胡桃醌诱导 GFP 表达。这与 DAF-16 向核内易位有关,如在表达 DAF-16::GFP 融合蛋白的转基因株系(TJ356)中观察到的那样,并且细胞内还原型谷胱甘肽水平增加。CL2070 中 DAF-16 的 RNA 干扰阻断了胡桃醌诱导的 HSP-16.2 表达和谷胱甘肽水平的增加。较高浓度的胡桃醌不会进一步增加适应性反应,但会导致过早死亡,表明存在激素适应,除非应激源超过内在的保护能力。添加 ROS 清除剂抗坏血酸最终阻止了寿命缩短和对胡桃醌应激的所有适应,这表明 ROS 确实是需要保护反应的分子种类。

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