Inhibition of ROS elevation and damage to mitochondrial function prevents lead-induced neurotoxic effects on structures and functions of AFD neurons in Caenorhabditis elegans  

作　　者：Qiuli Wu Peidang Liu Yinxia Li Min Du Xiaojuan Xing Dayong Wang 

机构地区：[1]Key Laboratory of Environmental Medicine Engineering in Ministry of Education,Medical School of Southeast University,Nanjing 210009,China [2]Department of Biochemistry and Molecular Biology,Medical School of Southeast University,Nanjing 210009,China

出　　处：《Journal of Environmental Sciences》2012年第4期733-742,共10页环境科学学报（英文版）

基　　金：supported by the National Basic Research Program (973) of China (No. 2011CB933404);and the National Natural Science Foundation of China (No.30870810,81172698);Some strains used were provided by Caenorhabditis Genetics Center (funded by the NIH National Center for Research Resource,USA)

摘　　要：Here we investigated the possible roles of oxidative stress in the formation of decreased thermotaxis to cultivation temperature in lead （Pb）-exposed nematodes Caenorhabditis elagans. Exposure to Pb at the examined concentrations decreased thermotaxis behaviors, and induced severe deficits in the structural properties of AFD sensory neurons. Meanwhile, Pb exposure caused the induction of severe oxidative damage, reactive oxygen species （ROS） production, and mitochondrial dysfunction in young adults. Moreover, pre-treatment with the antioxidants dimethyl sulfoxide （DMSO）, ascorbate and N-acetyl-L-cysteine （NAC）, used to inhibit both the ROS elevation and the mitochondrial dysfunction caused by Pb exposure, at the L2-1arval stage prevented the induction of oxidative damage and the formation of severe deficits in thermotaxis and structural properties of AFD sensory neurons in Pb-exposed young adults. Therefore, the formation of oxidative stress caused by Pb exposure may be due to both the induction of ROS elevation and damage to mitochondrial function, and oxidative stress may play a key role in inducing the neurotoxic effects on the structures and function of AFD sensory neurons in Pb-exposed nematodes.Here we investigated the possible roles of oxidative stress in the formation of decreased thermotaxis to cultivation temperature in lead （Pb）-exposed nematodes Caenorhabditis elagans. Exposure to Pb at the examined concentrations decreased thermotaxis behaviors, and induced severe deficits in the structural properties of AFD sensory neurons. Meanwhile, Pb exposure caused the induction of severe oxidative damage, reactive oxygen species （ROS） production, and mitochondrial dysfunction in young adults. Moreover, pre-treatment with the antioxidants dimethyl sulfoxide （DMSO）, ascorbate and N-acetyl-L-cysteine （NAC）, used to inhibit both the ROS elevation and the mitochondrial dysfunction caused by Pb exposure, at the L2-1arval stage prevented the induction of oxidative damage and the formation of severe deficits in thermotaxis and structural properties of AFD sensory neurons in Pb-exposed young adults. Therefore, the formation of oxidative stress caused by Pb exposure may be due to both the induction of ROS elevation and damage to mitochondrial function, and oxidative stress may play a key role in inducing the neurotoxic effects on the structures and function of AFD sensory neurons in Pb-exposed nematodes.

关 键 词：THERMOTAXIS lead exposure oxidative stress AFD sensory neuron Caenorhabditis elegans 

分 类 号：Q954.671[生物学—动物学] S826.1[农业科学—畜牧学]