Exposure to mercury causes formation of male-specific structural deficits by inducing oxidative damage in nematodes.
Metal exposure causes reproductive damage in hermaphrodite nematodes, but effects of metals on male development are unclear. We here investigated the effects of mercury chloride exposure on development of males. Hg exposure severely increased the percentage of abnormal males, disrupted the development of male-specific structures, and caused high reactive oxygen species (ROS) production in male tails. Pre-treatment with antioxidant (vitamin E) protected the nematodes against toxicity from Hg exposure on development of male-specific structures. The ROS production in tails was closely correlated with formation of abnormal male-specific structures in males induced by Hg exposure. Moreover, mutations of clk-1, encoding ortholog of COQ7/CAT5, and daf-2, encoding an insulin/IGF receptor, functioned in two different pathways to suppress the formation of deficits in development of male-specific structures. Thus, three different lines of evidence support our conclusion that HgCl(2) causes male structure-specific teratogenesis via production of oxidative stress.
Key Laboratory of Environmental Medicine Engineering in Ministry of Education, Medical School of Southeast University, Nanjing 210009, China; Department of Biochemistry and Molecular Biology, Medical School of Southeast University, Nanjing 210009, China; Institute of Neuroscience, Medical School of Southeast University, Nanjing 210009, China.
Peidang
P
Liu
Key Laboratory of Environmental Medicine Engineering in Ministry of Education, Medical School of Southeast University, Nanjing 210009, China; Department of Biochemistry and Molecular Biology, Medical School of Southeast University, Nanjing 210009, China.
Kewen
K
He
Key Laboratory of Environmental Medicine Engineering in Ministry of Education, Medical School of Southeast University, Nanjing 210009, China; Department of Biochemistry and Molecular Biology, Medical School of Southeast University, Nanjing 210009, China.
Yinxia
Y
Li
Key Laboratory of Environmental Medicine Engineering in Ministry of Education, Medical School of Southeast University, Nanjing 210009, China; Department of Biochemistry and Molecular Biology, Medical School of Southeast University, Nanjing 210009, China.
Qiuli
Q
Wu
Key Laboratory of Environmental Medicine Engineering in Ministry of Education, Medical School of Southeast University, Nanjing 210009, China; Department of Biochemistry and Molecular Biology, Medical School of Southeast University, Nanjing 210009, China.
Peng
P
Yang
Key Laboratory of Environmental Medicine Engineering in Ministry of Education, Medical School of Southeast University, Nanjing 210009, China; Department of Biochemistry and Molecular Biology, Medical School of Southeast University, Nanjing 210009, China. Electronic address: dayongw@seu.edu.cn.
Dayong
D
Wang
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D004785:Environmental Pollutants / Q000633:toxicity*; D008297:Male; D008628:Mercury / Q000633:toxicity*; D009348:Nematoda / Q000033:anatomy & histology / Q000187:drug effects* / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology
D000975:Antioxidants; D004785:Environmental Pollutants; D017382:Reactive Oxygen Species; D014810:Vitamin E; D008628:Mercury