Selenium as a protective agent against acrylamide-induced neurotoxicity and hepatotoxicity in rats
- سال انتشار: 1398
- محل انتشار: پانزدهمین همایش سراسری سم شناسی ایران
- کد COI اختصاصی: TOXICOLOGY15_030
- زبان مقاله: انگلیسی
- تعداد مشاهده: 432
نویسندگان
Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran- Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran- Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
چکیده
Introduction: Acrylamide (ACR) is a potent toxic agent, which has different applications in many industries. ACR induces toxicity in human and animals. Selenium is an essential trace element nutritionally important to mammals and has neuroprotective and hepatoprotective activities. Therefore, in the present study the probable protective effect of selenium on ACR-induced neurotoxicity and hepatotoxicity in rat was evaluated.Methods: Rats were divided into following groups: control (normal saline, i.p), ACR (50 mg/kg/day, i.p), selenium (0.2, 0.4 and 0.6 mg/kg, i.p ) plus ACR, vitamin E (200 mg/kg, i.p, every other day) plus ACR and selenium (0.6 mg/kg/day, i.p). At the end of treatment behavioral test was done. The levels of malondialdehyde (MDA) and glutathione (GSH) were determined spectrophotometrically. Apoptosis-involved factors including Bax, Bcl-2, and caspase3 proteins were evaluated using western blot method in the liver and brain tissues. Additionally, the biochemical parameters of albumin, total protein and hepatic enzymes of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured in serum.Results: Administration of ACR induced severe motor impairment in animals, elevated MDA level and reduced GSH content in liver and brain tissues in comparison to control group. In apoptosis pathway, the Bax/Bcl-2 ratio and caspase-3 protein increased in brain and liver tissues following exposure to ACR. The level of AST was elevated while the total serum protein and albumin content were decreased in ACR group as compared to control group. Administration of selenium (0.6 mg/kg) significantly recovered locomotor disorders, enhanced GSH content, reduced lipid peroxidation and decreased Bax/Bcl-2 ratio and caspase 3 protein levels in brain and liver tissues.Conclusion: ACR induced neurotoxicity and hepatotoxicity in rat through oxidative stress and apoptosis pathways. Selenium markedly inhibited ACR-induced toxicity via inhibition of oxidative stress and apoptosis.کلیدواژه ها
Acrylamide, Selenium, Oxidative stress, Apoptosisمقالات مرتبط جدید
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