Lactational exposure to inorganic mercury: evidence of neurotoxic effects

This study examined the effects of inorganic mercury (mercuric chloride - HgCl2) exposure exclusively through maternal milk on biochemical parameters related to oxidative stress (glutathione and thiobarbituric acid reactive substances levels, glutathione peroxidase and glutathione reductase activities) in the cerebellum of weanling mice. These parameters were also evaluated in the cerebellum of mothers, which were subjected to intraperitoneal injections of HgCl2 (0, 0.5 and 1.5 mg/kg, once a day) during the lactational period. Considering the relationship between cerebellar function and motor activity, the presence of motor impairment was also evaluated in the offspring exposed to HgCl2 during lactation. After treatments (at weaning), pups lactationally exposed to inorganic mercury showed high levels of mercury in the cerebellar tissue, as well as significant impairment in motor performance in the rotarod task and decreased locomotor activity in the open field. Offspring and dams did not show changes in cerebellar glutathione levels or glutathione peroxidase activity. In pups, lactational exposure to inorganic mercury significantly increased cerebellar lipoperoxidation, as well as the activity of cerebellar glutathione reductase. However, these phenomena were not observed in dams. These results indicate that inorganic mercury exposure through maternal milk is capable of inducing biochemical changes in the cerebellum of weanling mice, as well as motor deficit and these phenomena appear to be related to the pro-oxidative properties of inorganic mercury.