FACULTY OF VETERINARY MEDICINE

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Author: search.filters.author.Omobowale, T. O.Subject: search.filters.subject.Hepatotoxicity

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    Failure of recovery from lead induced hepatotoxicity and disruption of erythrocyte antioxidant defense system in Wistar rats
    (Elsevier B. V., 2014) Omobowale, T. O.; Oyagbemi, A. A.; Akinrinde, A. S.; Saba, A. B.; Daramola, O. T.; Ogunpolu, B. S.; Olopade, J. O.
    Lead acetate (PbA) is one of the major environmental contaminants with grave toxicological consequences both in the developing and developed countries. The liver and erythrocyte antioxidant status and markers of oxidative were assessed. Exposure of rats to PbA led to significant decline (p < 0.05) in hepatic and erythrocyte glutathione peroxidase (GPx), glutathione S-transferase (GST), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) content. Similarly, malondialdehyde (MDA) and H2O2 concentrations were significantly (p < 0.05) elevated. Histopathology and immunohistology of liver of rats exposed to PbA showed focal areas of necrosis and COX-2 expression after 6 weeks of PbA withdrawal. Taken together, hepatic and erythrocytes antioxidant defence system failed to recover after withdrawal of the exposed PbA for the period of the study. In conclusion, experimental animals exposed to PbA did not recover from hepatotoxicity and disruption of erythrocyte antioxidant defence system via free radical generation and oxidative stress.
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    Failure of recovery from lead induced hepatoxicity and disruption of erythrocyte antioxidant defence system in Wistar ratsTemidayo
    (Elsevier B.V., 2014) Omobowale, T. O.; Oyagbemi, A. A.; Akinrinde, A. S.; Saba, A. B.; Daramola, O. T.; Ogunpolu, B. S.; Olopade, J. O.
    Lead acetate (PbA) is one of the major environmental contaminants with grave toxicologicalconsequences both in the developing and developed countries. The liver and erythrocyteantioxidant status and markers of oxidative were assessed. Exposure of rats to PbA ledto significant decline (p < 0.05) in hepatic and erythrocyte glutathione peroxidase (GPx),glutathione S-transferase (GST), catalase (CAT), superoxide dismutase (SOD), and reducedglutathione (GSH) content. Similarly, malondialdehyde (MDA) and H2O2concentrations weresignificantly (p < 0.05) elevated. Histopathology and immunohistology of liver of rats exposedto PbA showed focal areas of necrosis and COX-2 expression after 6 weeks of PbA withdrawal.Taken together, hepatic and erythrocytes antioxidant defence system failed to recover afterwithdrawal of the exposed PbA for the period of the study. In conclusion, experimentalanimals exposed to PbA did not recover from hepatotoxicity and disruption of erythrocyteantioxidant defence system via free radical generation and oxidative stress.
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    Ameliorative effect of gallic acid in doxorubicin-induced hepatotoxicity in wistar rats through antioxidant defense system
    (Taylor & Francis, 2017-07) Omobowale, T. O.; Oyagbemi, A. A.; Ajufo, U. E.; Adejumobi, A. O.; Ola-Davies, O. E.; Adedapo, A. A.; Yakubu, M. A.
    Hepatotoxicity has been found to be one of the main side effects associated with doxorubicin (Dox) administration in cancer therapy. The aim of the present study was to examine the ameliorative effect of gallic acid (GA) in Dox-induced hepatotoxicity. Sixty male Wistar rats of 10 rats per group were used in this study and were randomly divided into 6 experimental groups (A–F). Rats in Group A served as the control group and received distilled water orally for 7 days; Group B was given Dox at 15 mg/kg bodyweight intraperitoneally (IP) on Day 8. Group Cwas given GA at 60 mg/kg body weight orally for 7 days + Dox at 15 mg/kg IP on Day 8. Group D was given GA at 120 mg/kg body weight orally for 7 days +Dox at 15 mg/kg IP on day 8. Rats in Groups E and F were administered GA alone at 60 and 120 mg/kg bodyweight orally for 7 days, respectively. Dox administration led to a significant reduction in hepatic reduced glutathione and nonprotein thiol (NPT) together with significant increase in hepatic malondialdehyde, hydrogen peroxide generation, superoxide dismutase, and catalase activity; hepatic glutathione peroxidase and glutathione-S-transferase activity were significantly inhibited in Dox-treated rats. The serum alanine aminotransferase (ALT), alkaline phosphatase, and total bilirubin concentrations were significantly elevated following Dox administration. Pretreatment with GA ameliorated Dox-induced hepatotoxicity and oxidative stress. The results suggest that GA may offer protection against hepatic damage in Dox cancer chemotherapy.