FACULTY OF VETERINARY MEDICINE

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    Effect of exposure and withdrawal on lead-induced toxicity and oxidative stress in cardiac tissues of rats
    (Society of Toxicology, India, 2016) Omobowale, T. O.; Oyagbemi, A. A.; Akinrinde, A. S.; Ola-Davies, O. E.; Saba, A. B.; Olukayode, O. J.; Adeolu, A. A.
    Lead poisoning continues to pose a serious health challenge and more significantly so in developing countries with ineffective waste disposal systems. Recent efforts at solving lead poisoning issues have seen entire towns being resettled from lead-contaminated areas. This study was designed to investigate whether withdrawal of lead exposure results in a resolution of toxic effects of lead in cardiac tissues. Adult male Wistar rats were exposed orally to lead acetate (PbA) at doses of 0.25, 0.5, and 1.0 mg/ml for 6-week duration, after which one-half was sacrificed and the remaining left for a further 6 weeks without lead treatment. Exposure of rats to PbA produced significant decline (P < 0.05) in the activities of antioxidant parameters, including superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), catalase (CAT), and reduced glutathione (GSH), whereas malondialdehyde (MDA) concentration was significantly elevated. Animals from the withdrawal period exhibited a similar pattern of alterations, with a significant (P < 0.05) reduction in GSH, GPx, and SOD and a significant elevation in MDA and H2O2 concentrations. However, GST activity was elevated, whereas CAT activity remained unaltered in the withdrawal period. The results of this study showed that cardiotoxicity indicated by induction of oxidative stress and reduction in antioxidant parameters failed to resolve upon withdrawal of lead exposure in male rats during the period of study.
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    The toxic effects of the prolonged administration of chloramphenicol on the liver and kidney of rats
    (Biomedical Communications Group, Ibadan, Nigeria, 2000) Saba, A. B.; Ola-Davies, O.; Oyeyemi, M. O.; Ajala, O.
    The toxic effect of chloramphenicol on the liver and kidney was studied in laboratory Wistar rats. 16 adult rats of both sexes randomly divided into two groups were used. 10 animals in the test group were administered with chloramphenicol orally using rat cannula at human infant recommended dosage of 25mg/kg body weight given once daily for a period of 16 days. The 6 animals in the control group were only administered with 0.9% physiological saline orally over the same period of time. Serum enzymes and levels of serum bilirubin, urea, and creatinine were evaluated to establish any hepatic or renal dysfunction. There was statistically significant increase in aspartate aminotransferase (P<0.05) and alanine aminotransferase (P<0.001) serum levels in the test animals. The increase in serum alkaline phosphatase was not statistically significant (P>0.05). Hyperbilirubinaemia was observed in the rat administered with chloramphenicol, the difference in the mean value of the test and control animals were significant for total and conjugated bilirubin. (Total bilirubin P<0.01; Conjugated bilirubin P<0.05). The average time taken to establish anaesthesia was shorter in the test animals than in animals in the control group, the difference in the mean values was significant (P<0.05). Serum urea and creatinine levels were elevated in the test animals, the increase is only statistically significant for serum urea (P<0.05) but not significant for creatinine (P>0.05). Histopathology revealed vascular congestion and foamy cytoplasm of hepatocytes at the centrilobular region of the liver but did not reveal any damage done to the renal tissue. It was concluded that chloramphenicol may not be nephrotoxic but may have toxic effects on the liver.