FACULTY OF VETERINARY MEDICINE

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Author: search.filters.author.Ola-Davies, O. E.Subject: search.filters.subject.Hepatotoxicity

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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.
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    Modulatory effects of guava extract on adriamycin (doxorubicin) induced toxicity in wistar rats
    (IDOSI Publications, 2016) Ola-Davies, O. E.; Azeez, O.
    Adriamycin, though, a drug of choice in cancer therapy, its use is associated with acute and chronic complications, which are capable of exacerbating the conditions of the patients. Thus, efforts are being directed at evaluating several compounds, antioxidants and natural products that are capable of ameliorating these complications whilst still retaining the potency and efficacy of Adriamycin as an anti cancer agent. The modulatory and ameliorative effects of methanol guava leaf extract (Psidium guajava Linn) against Adriamycin/Doxorubicin toxicity was evaluated in Wistar rats. Adriamycin (ADR) injection resulted in considerable liver and kidney damage as seen in the form of elevated liver enzymes, total protein as well as urea and creatinine levels in the blood. It also resulted in increases in the total triglyceride and cholesterol levels. The use of the extract alone on the other hand showed hepatoprotective and nephroprotective properties of guava leaf extract in that the above parameters were significantly lower than those of the untreated control. The protective effect of the extract against ADR toxicity was however limited to the liver. Effects which, may be due to the antioxidant and free radical scavenging properties of some of the components of the extract.
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    Chemoprevention of aflatoxin B1-induced genotoxicity and hepatic oxidative damage in rats by kolaviron, a natural biflavonoid of garcinia kola seeds
    (Lippincott Williams & Wilkins, 2005) Farombi, E. O.; Adepoju, B. F.; Ola-Davies, O. E.; Emerole, G. O.
    The chemopreventive effects of kolaviron, a natural antioxidant biflavonoid from the seeds of Garcinia kola, on aflatoxin B1 (AFB1)-induced genotoxicity and hepatic oxidative damage was investigated in rats. Kolavironmadministered orally at a dose of 200 mg/kg once a day for the first 2 weeks and then 100 mg/kg twice a day for the last 4 weeks of AFB1 (2 mg/kg, single dose, intraperitoneal) treatment reduced the AFB1-increased activities of aspartate amino transferase (AST), alanine amino transferase (ALT) and gamma glutamyltransferase (c-GT) by 62%, 56% and 72% respectively. Malondialdehyde (MDA) formation and lipid hydroperoxide (LHP) accumulation were observed in the livers of AFB1-treated rats. Kolaviron significantly reduced the AFB1-induced MDA and LHP formation. Vitamins C and E were protective in reducing the increase in the activities of AST, ALT and c-GT as well as lipid peroxidation caused by AFB1 (P < 0.01). Administration of rats with kolaviron alone resulted in significant elevation in the activities of glutathione S-transferase, uridyl glucuronosyl transferase and NADH:quinone oxidoreductase by 2.45-, 1.62- and 1.38-folds respectively. In addition, kolaviron attenuated the AFB1-mediated decrease in the activities of these enzymes (P < 0.01). Pretreatment of rats with kolaviron, vitamins C and E alone did not exert genotoxicity assessed by the formation of micronucleated polychromatic erythrocytes (MNPCEs) (P> 0.05). Co-treatment of rats intraperitoneally with kolaviron (500 mg/kg) 30 min before and 30 min after AFB1 (1 mg/kg) administration inhibited the induction of MNPCEs by AFB1 (P < 0.001) after 72 h. While vitamin C was effective in reducing AFB1- induced MNPCEs formation, vitamin E did not elicit any antigenotoxic response. These results indicate kolaviron as effective chemopreventive agent against AFB1-induced genotoxicity and hepatic oxidative stress. Thus kolaviron may qualify for clinical trial in combating the menace of aflatoxicosis in endemic areas of aflatoxin contamination of foods.