FACULTY OF VETERINARY MEDICINE

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    Cobalt chloride exposure dose dependently induced hepatotoxicity through enhancement of cyclooxygenase-2 (COX-2)/B- cell associated protein X (BAX) signaling and genotoxicity in wistar rats
    (Wiley, 2017-02) Awoyemi, O. V.; Okotie, U. J.; Oyagbemi, A. A.; Omobowale, T. O.; Asenuga, E. R.; Ola-Davies, O. E.; Ogunpolu, B. S.
    Cobalt chloride (CoCl2) is one of the many environmental contaminants, used in numerous industrial sectors. It is a pollutant with deadly toxicological consequences both in developing and developed countries. We investigated toxicological impact of CoCl2 on hepatic antioxidant status, apoptosis, and genotoxicity. Forty Wistar rats were divided into four groups, 10 rats per group: Group 1 served as control and received clean tap water orally; Group 2 received CoCl2 solution (150 mg/L); Group 3 received CoCl2 solution (300 mg/L); and Group 4 received CoCl2 (600 mg/L) in drinking water for 7 days, respectively. Exposure of rats to CoCl2 led to a significant decline in hepatic antioxidant enzymes together with significant increase in markers of oxidative stress. Immunohistochemistry revealed dose-dependent increase in cyclooxygenase-2 and BAX expressions together with increased frequency of Micronucleated Polychromatic Erythrocytes. Combining all, CoCl2 administration led to hepatic damage through induction of oxidative stress, inflammation, and apoptosis.
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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.