Cadmium (Cd), a well-known environmental pollutant, widely exists in water, soils, sediments, and air, and produces various system dysfunctions including those affecting the nervous system. L-carnitine (L-CAR) is an antioxidant that plays neuroprotective roles by improving enzyme functions. The purpose of our study was to evaluate whether L-CAR could efficiently protest against neurotoxicity induced by Cd. Rats were exposed to different concentrations of Cd (0, 25, 50, 100 mg/l) for 4 weeks. We used the open-field test (OFT) and forced-swimming test (FST) to observe the rats'spontaneous locomotor activity and exploration behavior; brain histopathological section to observe the damage of cortical neurons in the brain; Oxidative stress indicators reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) were determined at terminal time-points. The protective effects of L-CAR(1.5 g/l) were evaluated in parallel. Here, we corroborated that that L-CAR is a potential pharmacological agent that protests against the neurotoxicity of Cd. The results of brain histopathological sections show that with the increase of cadmium dosage in drinking water, but the damage to cortical neurons becomes more severe;the Cd(100 mg/l) + L-CAR(1.5 g/l) group, the neuronal cell membrane was intact, the cell outline was clear. The Cd-induced oxidative stress in the cerebral cortex was proven by elevation of ROS, MDA levels, and reduction of SOD activity. However, those effects on oxidative stress were attenuated if L-CAR(1.5 g/l) was simultaneously administrated. The results suggested that L-CAR is a potential pharmacological agent that protects the neurotoxicity of Cd.
Wang et al. (Sat,) studied this question.