This study examined the exclusive contribution of mercury chloride (HgCl2) exposure 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 suckling mice.
The same biochemical parameters were also evaluated in the cerebellum of mothers, which were submitted to i.p. injections of HgCl2 (0, 0.5 and 1.5 mg/Kg). Considering the relationship between cerebellar function and motor activity, the presence of signs of motor impairment was also evaluated in the offspring exposed to HgCl2 during lactation.
After the treatment (at weaning period), the pups lactationally exposed to HgCl2 showed significant impairment in the motor performance observed in the rotarod task and decreased locomotor activity in the open field. In addition, offspring and dams had not shown changes on glutathione levels and glutathione peroxidase activity in the cerebellum. In pups, HgCl2 significantly increased cerebellar lipoperoxidation and the activity of cerebellar glutathione reductase. However, these phenomena were not observed in dams.
This study indicates that the exposure of lactating mice to HgCl2 causes significant impairments in the motor performance in the offspring and this phenomenon may be related to the oxidative effects of HgCl2 in the cerebellum.
Keywords: mercury chloride, lactational exposure, neurotoxicity, TBARS, oxidative stress, antioxidant enzymes, motor impairment.