4.6

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2.2

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  • ISSN 1674-8301
  • CN 32-1810/R
Iyaswamy Ashok, Rathinasamy Sheeladevi, Dapkupar Wankhar. Acute effect of aspartame-induced oxidative stress in Wistar albino rat brain[J]. The Journal of Biomedical Research, 2015, 29(5): 390-396. DOI: 10.7555/JBR.28.20120118
Citation: Iyaswamy Ashok, Rathinasamy Sheeladevi, Dapkupar Wankhar. Acute effect of aspartame-induced oxidative stress in Wistar albino rat brain[J]. The Journal of Biomedical Research, 2015, 29(5): 390-396. DOI: 10.7555/JBR.28.20120118

Acute effect of aspartame-induced oxidative stress in Wistar albino rat brain

More Information
  • Received Date: October 05, 2012
  • Revised Date: November 12, 2012
  • The present study was carried out to investigate the acute effect of aspartame on oxidative stress in the Wistar albino rat brain. We sought to investigate whether acute administration of aspartame (75 mg/kg) could release methanol and induce oxidative stress in the rat brain 24 hours after administration. To mimic human methanol metabolism, methotrexate treated rats were used to study aspartame effects. Wistar strain male albino rats were administered with aspartame orally as a single dose and studied along with controls and methotrexate treated controls. Blood methanol and formate level were estimated after 24 hours and rats were sacrificed and free radical changes were observed in discrete regions by assessing the scavenging enzymes, reduce dglutathione (GSH), lipid peroxidation and protein thiol levels. There was a significant increase in lipid peroxidation levels, superoxide dismutase activity (SOD), glutathione peroxidase levels (GPx), and catalase activity (CAT) with a significant decrease in GSH and protein thiol. Aspartame exposure resulted in detectable methanol even after 24 hours. Methanol and its metabolites may be responsible for the generation of oxidative stress in brain regions. The observed alteration in aspartame fed animals may be due to its metabolite methanol and elevated formate. The elevated free radicals due to methanol induced oxidative stress.
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