Abstract

Background. In the recent years, extensive research work has been focused on the use of natural materials as antioxidants against the toxic oxidative materials to ameliorate their toxic and cell damaging effects. Aim. To evaluate the antioxidant effects of bee honey and propolis against OA-induced oxidative stress in liver and kidney in rats. Materials and Methods. 64 albino rats divided into 8 groups, group 1 as control, groups 2 - 4 received an oral dose of OA, honey and propolis respectively for four weeks, groups 5 and 6 were treated with a weekly dose of OA concomitant with a daily dose of bee honey in group 5 and propolis in group 6, groups 7and 8 were treated with a daily dose of bee honey in group 7 and propolis in group 8 and single weekly dose of OA then adminstrered starting the second week of treatment. After 4 weeks, blood samples, liver and kidney tissues were collected for the subsequent determinations. Results. The study showed that OA exerted toxic effects on both liver and kidney tissues manifested as elevated serum alanine aminotransferase (ALT), gamma glutamyl transferase (γ GT), creatinine and cholestrol. OA also caused perturbation in liver and kidney antioxidant system reflected as diminished reduced glutathione (GSH), oxidized glutathione (GSSG) content and also decrease in glutathione peroxidase (GPX) and superoxide dismutase (SOD) activity. The level of malondialdehyde (MDA) which is a lipid peroxidation product was elevated. Bee honey (BH) and propolis (PR) ameliorated the toxic effects of OA on liver and kidney tissues with significant reduction of mean serum levels of ALT, γ GT, cholesterol and creatinine. Also BH and PR improved the reduction in the antioxidant parameters of the liver and kidney (GSH, GSSG content and GPX , SOD activity) caused by OA administration. The level of MDA was also significantly decreased. Conclusion. Bee honey and propolis ameliorated OA-induced oxidative stress in the liver and kidney through their role in scavenging free radicals and preventing lipid peroxidation.

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