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 HgCl2 causes male structure-specific teratogenesis via production of oxidative stress.

► Hg exposure induced defects of male-specific structures and ROS production in tails.
► Antioxidant pretreatment protected against Hg toxicity on male-specific structures.
► ROS production in tails was correlated with Hg-induced male structural defects.
► clk-1 and daf-2 functioned parallel to suppress male structural defects formation.
► Mercury caused male structure-specific teratogenesis via oxidative stress production.