Protective effects of selenium on acrylamide-induced neurotoxicity and hepatotoxicity in rats

Objective(s): Acrylamide (ACR), has wide uses in different industries. ACR induced several toxicities including neurotoxicity and hepatotoxicity. The probable protective effects of selenium on ACR-induced neurotoxicity and hepatotoxicity in rats were evaluated.Materials and Methods: Male Wistar rats were studied for ۱۱ days in ۸ groups: ۱. Control, ۲. ACR (۵۰ mg/kg, IP), ۳-۵. ACR+ selenium (۰.۲, ۰.۴, ۰.۶ mg/kg, IP), ۶. ACR+ the most effective dose of selenium (۰.۶ mg/kg, IP) three days after ACR administration, ۷. ACR+ vitamin E (۲۰۰ mg/kg IP, every other day) ۸. Selenium (۰.۶ mg/kg IP). Finally, behavioral tests were done. The levels of malondialdehyde (MDA), glutathione (GSH), Bcl-۲, Bax and caspase ۳ 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-۲ ratio and caspase ۳ 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 (۰.۶ 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-۲ ratio and caspase ۳ levels in brain and liver tissues.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.

کلیدواژه ها:

Acrylamide ، Apoptosis ، Hepatotoxicity ، Neurotoxicity ، Oxidative stress ، Selenium