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.

Cerebellar thiol status and motor deficit after lactational exposure to methylmercury.

This study examined the exclusive contribution of methylmercury (MeHg) exposure through maternal milk on biochemical parameters related to the thiol status (glutathione (GSH) levels, glutathione peroxidase (GPx) and glutathione reductase (GR) activities) in the cerebellums of suckling mice. The same biochemical parameters were also evaluated in the cerebellums of mothers, which were submitted to a direct oral exposure to MeHg (10 mg/L in drinking water). With regard to the relationship between cerebellar function and motor activity, the presence of signs of motor impairment was also evaluated in the offspring exposed to MeHg during lactation. After the treatment (at weaning period), the pups lactationally exposed to MeHg showed increased levels of mercury in the cerebellum compared to pups in the control group and a significant impairment in the motor performance in the rotarod apparatus. In addition, these pups showed decreased levels of GSH in the cerebellum compared to pups in the control group. In dams, MeHg significantly increased the levels of cerebellar GSH and the activities of cerebellar GR. However, this was not observed in pups. This study indicates that (1) the exposure of lactating mice to MeHg causes significant impairments in motor performance in the offspring which may be related to a decrease in the cerebellar thiol status and (2) the increased GSH levels and GR activity, observed only in the cerebellums of MeHg-exposed dams, could represent compensatory pathophysiologic responses to the oxidative effects of MeHg toward endogenous GSH.