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Tanta Medical Journal. 1998; 26 (Supp. 1): 611-30
in English | IMEMR | ID: emr-49910

ABSTRACT

The assumption of oxidative stress as a mechanism in lead [Pb] toxicity suggests that antioxidants might play a role in the prevention or treatment of lead poisoning. This study was conducted to evaluate the neuroprotective effect of the dietary curcumin [Cur] using Pb-exposed rats as a model of brain injury. Male albino rats were divided into four groups; the first was the control group received saline, the second was Pb-group given intragastric 5 mg.lead acetate/kg daily,the third was Pb-Cur group subjected to combined administration of Cur and lead acetate. Cur was given intragastrically at a dose of 50 mg/kg 2h prior to each dose of lead acetate. The fourth group was Cur group given only Cur [50 mg/kg/day]. Second, third and fourth groups were further divided into 3 subgroups that received the assigned treatments for 2, 4 and 6 weeks [w], respectively. The results showed that Pb group exhibited neurotoxicity manifested by the inhibited enzymatic activities of hexokinase, acetylcholinesterase and monoamine oxidase in rat brain. This Pb-induced neurotoxicity was accompanied by increased levels of lipid peroxidation and the ratio of oxidized glutathione to reduced glutathione in brain homogenates. Moreover, Immunohistochemistry showed that there was neuronal expression of inducible nitric oxide synthase [iNOS] in Pb-exposed rats started at 2w onwards and the histopathological examination also revealed minute cystic spaces at 2 and 4w but extensive cystic spaces, gliosis and marked neuronal loss after 6w of Pb treatment. The dietary antioxidant curcumin imparted a protective effect to the nervous system; it prevented lipid peroxidation, replenished the depleted reduced glutathione and inhibited expression of iNOS in Pb-Cur group at all time intervals. However, curcumin administration to Pb-treated rats, although significantly prevented the decrease in brain hexokinase, acetylcholinesterase and monoamine oxidase activities at 2w, failed to protect against Pb-induced damage at 4 and 6w. Curcumin could, therefore, prevent Pb-induced oxidative stress and protect against neuronal membrane injury. Curcumin may also restore brain enzymatic activities only when exposed to Pb for short periods but cannot counteract Pb-induced degeneration by long time exposure


Subject(s)
Animals, Laboratory , Immunochemistry , Lead Poisoning, Nervous System , Biomarkers , Animals, Laboratory , Hexokinase , Rats
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