Please use this identifier to cite or link to this item: http://ir.library.ui.edu.ng/handle/123456789/2964
Title: Influence of Chloramphenicol and Amoxicillin on Rat Liver Microsomal Enzymes and Lipid Peroxidation
Authors: Adesanoye, O. A.
Ifezue, A. O. C.
Farombi, E. O.
Keywords: Chloramphenicol
amoxicillin
lipid peroxidation
Ca2+-ATPase
glucose -6-phosphatase.
Issue Date: Sep-2014
Abstract: Generation of reactive oxygen species beyond the antioxidant capacity of biological system has been reported to give rise to oxidative stress which through a series of events deregulates cellular functions, leading to oxidative damage and various pathological conditions. This study examined the effect of chloramphenicol and amoxicillin on liver microsomal enzymes Ca2+-ATPase and Glucose-6-Phosphatase (G-6-P) and lipid peroxidation in rats. Male Wistar strain rats weighing 120 – 195 g were divided into four groups. Group one, the control group, received physiological saline, group two received Amoxicillin at 10.71 mg/kg, group three received Chloramphenicol at 28.57 mg/kg, while group four was administered combination of chloramphenicol and amoxicillin. Drugs were administered for ten days and the animals sacrificed on the eleventh day. Detection of oxidation in liver microsomal fraction was carried out by assessment of lipid peroxidation and conjugated diene. Ca2+-ATPase and G-6-P activities and total protein content were also measured. Data were analysed by ANOVA and Student’s T-Test. Significant (p<0.05) decreases in G-6-P activity by 55.30%, 38.37%, 55.30% and Ca2+-ATPase activity by 38.99%, 30.16%, 26.88% were recorded with chloramphenicol, amoxicillin and chloramphenicol/amoxicillin treatments respectively when compared with the control group while total microsomal protein content was depleted by 70.50% 79.27%, 75.87% respectively. TBARS and Diene Conjugation were significantly (p<0.05) elevated in the treated groups. Findings from this study suggest that Chloramphenicol and Amoxicillin induced oxidative stress in rats and perturbed Ca2+ homeostasis presumably due to generation of free radicals.
URI: http://ir.library.ui.edu.ng/handle/123456789/2964
ISSN: 1119-5096
Appears in Collections:scholarly works

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