Conclusion
The oxidative stress and apoptosis pathways have important roles in neurotoxicity and hepatotoxicity of ACR. Selenium significantly reduced ACR-induced toxicity through inhibition of oxidative stress and apoptosis.
Methods
Male Wistar rats were studied for 11 days in 8 groups: 1. Control, 2. ACR (50 mg/kg, IP), 3-5. ACR+ selenium (0.2, 0.4, 0.6 mg/kg, IP), 6. ACR+ the most effective dose of selenium (0.6 mg/kg, IP) three days after ACR administration, 7. ACR+ vitamin E (200 mg/kg IP, every other day) 8. Selenium (0.6 mg/kg IP). Finally, behavioral tests were done. The levels of malondialdehyde (MDA), glutathione (GSH), Bcl-2, Bax and caspase 3 proteins in liver and cerebral cortex tissues were measured. Also, the amount of albumin, total protein, alanine transaminase (ALT) and aspartate transaminase (AST) enzymes were determined in serum.
Results
ACR caused the severe motor impairment, increased MDA level and decreased GSH content, enhanced Bax/Bcl-2 ratio and caspase 3 proteins in brain and liver tissues. Besides, the level of AST was elevated while the total serum protein and albumin levels were decreased. Administration of selenium (0.6 mg/kg) (from the first day of the experiment and the third day) significantly recovered locomotor disorders, increased GSH content, and reduced MDA level. Also, selenium decreased Bax/Bcl-2 ratio and caspase 3 levels in brain and liver tissues.