Zinc attenuates malathion-induced depressant-like behavior and confers neuroprotection in the rat brain.

Malathion is an organophosphate widely used as an insecticide in agriculture and in public health programs, causing risk to human health. As was recently reported, malathion induces depressant-like behavior and oxidative damage to the brain of rodents. Given the relevance of searching for neuroprotective agents against such damage, this study was therefore undertaken to investigate the neuroprotective potential of zinc in dealing with malathion-related toxicity. Female Wistar rats were exposed to malathion (50 and 100 mg/kg, ip) and/or zinc chloride (ZnCl2; 5 mg/kg, ip) for 3 days. Malathion produced a depressant-like effect, observed by the increased immobility time in the forced swimming test (FST), without affecting total locomotor activity and rearing in the open-field. However, malathion administered at 50 mg/kg reduced the central time in the arena and at the dose of 100 mg/kg reduced the central locomotion. These effects were completely reversed by ZnCl2. Exposure to malathion (50 mg/kg, ip) and/or ZnCl2 did not affect AChE activity in the hippocampus, cerebral cortex, and blood. Malathion (50 mg/kg, ip) alone caused some harmful effects, such as (1) an increase in lipid peroxidation and a reduction of glutathione peroxidase activity in the cerebral cortex, (2) reduction of glutathione reductase activity in the hippocampus, and (3) changes in the structure of chromatin in the dentate gyrus, all effects attenuated by ZnCl2. In conclusion, these results clearly show that zinc administration is able to attenuate some neurochemical, morphological, and behavioral effects induced by malathion, notably the malathion-induced depressant-like effect in the FST.