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ZENG Li-ai, GUO Xiong-xiong, YAN Han-ying, . Interference effect of melatonin on acrylamide-induced neurotoxicity in rats[J]. Chinese Journal of Public Health, 2012, 28(2): 191-193. DOI: 10.11847/zgggws-2012-28-02-28
Citation: ZENG Li-ai, GUO Xiong-xiong, YAN Han-ying, . Interference effect of melatonin on acrylamide-induced neurotoxicity in rats[J]. Chinese Journal of Public Health, 2012, 28(2): 191-193. DOI: 10.11847/zgggws-2012-28-02-28

Interference effect of melatonin on acrylamide-induced neurotoxicity in rats

  • Objective To explore the interference effect of melatonin on acrylamide-induced neurotoxicity in rats. Methods Forty adult male SD rats were randomly divided into control group,acrylamide group,melatonin group,and melatonin intervention group(10 in each group).Acrylamide group was treated with 2.3 mmol/L of acrylamide in daily drinking.Rats in melatonin group were administered 2.5 mg/kg of melatonin by intraperitoneal injection once a day.All the treatments continued 9 weeks.Gait scores were analyzed once a week.The histopathologial injuries of cerebrum and cerebellum were observsed by hematoxhlin-eosin(HE)stain.The contents of of malondialdehyde(MDA),glutathione(GSH), superoxide dismutase(SOD),and glutathione peroxidase(GSH-Px)in cerebral cortex and cerebellum tissue were determined. Results Compared with the control group,the gait scores rised markedly from the third week to the end of experiment(P<0.05)in acrylamide group and melatonin intervention group.In acrylamide group,the SOD activity in cerebral cortex decreased by 9.89% (P<0.05)and the SOD activity and GSH content in cerebellum decreased by 7.49% and 12.31%,respectively(P<0.05).Compared with acrylamide group,gait scores decreased at forth and fifth week by 22.92% and 15.85%,respectively(P<0.05),and the SOD activity in cerebral cortex increased by 14.96% in melatonin intervention group(P<0.01). Conclusion Acrylamide could induce gait abnormality,inhibit the activity of SOD and the content of GSH,while melatonin could alleviate the neurotoxicity induced by acrylamide at the early stage but have no protective effect later in rats.
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