Effect of Restraint Stress and Cadmium Chloride Administration on Cerebral Antioxidants in Female Wistar Rats

Cadmium is a toxic heavy metal which promotes oxidative stress in various organs including the brain. Restraint stress is a model of stress which involves physical constraint to induce homeostatic imbalance. This study aimed to evaluate the interaction of restraint stress and cadmium toxicity on cerebral antioxidants in female Wistar rats. 24 female Wistar rats (180-220g) were randomly divided into 4 groups (n=6 each): Control (CTL), Restraint stress alone (RSS), Cadmium alone (CCC), Cadmium + Restraint stress (RSC). The experimental groups were subjected to cadmium chloride 100mg/kg b.w. orally and restraint stress for 30 minutes using wire mesh. 24 hours post last cadmium administration and restraint stress exposure, all animals were anaesthetized and sacrificed. The brain was excised, homogenized and analyzed for antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase), lipid peroxidation (Malondialdehyde). Results showed that there was significant (p<0.05) decrease in superoxide dismutase in cadmium alone and restraint stress alone groups when compared to control. In the restraint stress alone and cadmium alone groups, cerebral catalase was significantly (p˂0.05) decreased when compared to Control. Additionally, a marked (p˂0.05) decrease in catalase activity was observed in cadmium + restraint group when compared to restraint stress alone and Cadmium alone groups. Furthermore, cadmium exposure led to a notable (p˂0.05) decrease in cerebral glutathione peroxidase when compared to control. The combined exposure to cadmium and restraint stress significantly (p˂0.05) decreased cerebral glutathione peroxidase when compared to restraint stress and Cadmium alone groups. In the cadmium alone group, there was a pronounced (p<0.05) increase in Malondialdehyde when compared to the control group. In conclusion, this present study have shown that combined exposure to cadmium and restraint stress increased free radical production and significantly decreased antioxidant system indicating that combined mechanism of both factors adversely induced neurological damage.