Key Laboratory of Developmental Genes and Human Disease in Ministry of Education, Institute of Life Sciences, Southeast University, Nanjing 210009, China.
Ecotoxicol Environ Saf. 2010 Sep;73(6):1221-30. doi: 10.1016/j.ecoenv.2010.05.002. Epub 2010 Jun 30.
We investigated the possible formation of combined toxicity from Ca/Cd exposure on nematode lifespan. Ca exposure at concentrations more than 1.56 mM significantly reduced lifespan, accelerated aging-related declines, and induced severe stress response in wild-type nematodes. Combined Ca (25 mM)/Cd (200 microM) exposure decreased the lifespans compared to Cd (200 microM) exposure; whereas no lifespan differences were found between Ca (1.56 mM)/Cd (200 microM) exposure and Cd (200 microM) exposure. Combined Ca (25 mM)/Cd (200 microM) exposure caused a more significant induction of hsp-16.2::gfp expression, and a more severe increase in oxidative damage than Cd (200 microM) exposure. Moreover, mutation of mev-1, encoding a subunit of succinate dehydrogenase cytochrome b, enhanced the combined Ca/Cd toxicity on lifespan. Furthermore, mutation of daf-16, encoding a fork-head-family transcription factor, enhanced the combined Ca/Cd toxicity on lifespan, and mutation of daf-2, encoding an insulin receptor-like protein, alleviated the combined Ca/Cd toxicity on lifespan.
我们研究了 Ca/Cd 暴露对线虫寿命可能产生的联合毒性。暴露于浓度超过 1.56mM 的 Ca 显著缩短了线虫的寿命,加速了与衰老相关的下降,并诱导了野生型线虫的严重应激反应。与 Cd(200μM)暴露相比,Ca(25mM)/Cd(200μM)联合暴露降低了寿命;而 Ca(1.56mM)/Cd(200μM)暴露与 Cd(200μM)暴露之间没有寿命差异。Ca(25mM)/Cd(200μM)联合暴露引起 hsp-16.2::gfp 表达的诱导更为显著,氧化损伤的增加也比 Cd(200μM)暴露更为严重。此外,编码琥珀酸脱氢酶细胞色素 b 亚基的 mev-1 突变增强了 Ca/Cd 联合毒性对寿命的影响。此外,编码叉头家族转录因子的 daf-16 突变增强了 Ca/Cd 联合毒性对寿命的影响,而编码胰岛素受体样蛋白的 daf-2 突变减轻了 Ca/Cd 联合毒性对寿命的影响。