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首页> 外文期刊>Mitochondrion >Effects of reduced mitochondrial DNA content on secondary mitochondrial toxicant exposure in Caenorhabditis elegans
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Effects of reduced mitochondrial DNA content on secondary mitochondrial toxicant exposure in Caenorhabditis elegans

机译：线粒体DNA含量降低对秀丽隐杆线虫继发线粒体毒物暴露的影响

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The mitochondrial genome (mtDNA) is intimately linked to cellular and organismal health, as demonstrated by the fact that mutations in and depletion of mtDNA result in severe mitochondrial disease in humans. However, cells contain hundreds to thousands of copies of mtDNA, which provides genetic redundancy, and creates a threshold effect in which a large percentage of mtDNA must be lost prior to clinical pathogenesis. As certain pharmaceuticals and genetic mutations can result in depletion of mtDNA, and as many environmental toxicants target mitochondria, it is important to understand whether reduced mtDNA will sensitize an individual to toxicant exposure. Here, using ethidium bromide (EtBr), which preferentially inhibits mtDNA replication, we reduced mtDNA 35-55% in the in vivo model organism Caenorhabditis elegans. Chronic, lifelong, low-dose EtBr exposure did not disrupt nematode development or lifespan, and induced only mild alterations in mitochondrial respiration, while having no effect on steady-state ATP levels. Next, we exposed nematodes with reduced mtDNA to the known and suspected mitochondrial toxicants aflatoxin B-1, arsenite, paraquat, rotenone or ultraviolet C radiation (UVC). EtBr pre-exposure resulted in mild sensitization of nematodes to UVC and arsenite, had no effect on AfB(1) and paraquat, and provided some protection from rotenone toxicity. These mixed results provide a first line of evidence suggesting that reduced mtDNA content may sensitize an individual to certain environmental exposures. (C) 2016 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
机译：线粒体基因组（mtDNA）与细胞和机体健康密切相关，事实证明mtDNA的突变和耗竭会导致人类严重的线粒体疾病。然而，细胞包含数百至数千个mtDNA拷贝，这提供了遗传冗余，并产生了阈值效应，在这种阈值效应中，临床发病机理之前必须丢失大量的mtDNA。由于某些药物和基因突变会导致mtDNA耗竭，并且由于许多环境毒物靶向线粒体，因此重要的是要了解mtDNA降低是否会使个体对毒物暴露敏感。在这里，使用优先抑制mtDNA复制的溴化乙锭（EtBr），我们在体内模型生物秀丽隐杆线虫中降低了mtDNA 35-55％。长期，终身，低剂量的EtBr暴露不会破坏线虫的发育或寿命，并且仅诱导线粒体呼吸的轻度变化，而对稳态ATP水平没有影响。接下来，我们将线粒体含量降低的线虫暴露于已知和怀疑的线粒体毒物黄曲霉毒素B-1，亚砷酸盐，百草枯，鱼藤酮或紫外线C辐射（UVC）。 EtBr的预暴露导致线虫对UVC和亚砷酸盐的轻度敏化，对AfB（1）和百草枯没有影响，并提供了一些防止鱼藤酮毒性的保护作用。这些混杂的结果提供了第一线证据，表明降低的mtDNA含量可能会使个人对某些环境暴露敏感。 （C）2016 Elsevier B.V.和线粒体研究学会。版权所有。

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