Biochemistry
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Item Lack of recovery from hepatic oxidative damage in rats treated with Nigerian bonny light crude oil(John Wiley & Sons, Ltd., 2012) Adedara, I. A.; Farombi, E. O.The use of Nigerian bonny light crude oil (BLCO) in the treatment of gastrointestinal disorders, burns, foot ulcers and reproductive capacity is a common practice in the southern part of Nigeria. Towards understanding the mechanism and the reversibility of hepatotoxicity induced by BLCO, adult male Wistar rats were orally administered with BLCO at 0, 50, 100 and 200 mg kg 1 for 21 days. One-half of the rats were sacrificed on day 22, whereas the remaining half stayed for an additional 21 days without treatment. Whereas the activities of antioxidant enzymes such as superoxide dismutase, catalase, glutathione S-transferase were significantly (p<0.05) increased, gamma glutamyl transferase activity was significantly decreased in a dose-dependent manner. The levels of glutathione, hydrogen peroxide and malondialdehyde were significantly elevated in BLCO-treated animals. In addition, hepatic degeneration was accompanied with elevation in serum aminotransferases activities without affecting bilirubin levels. Whereas most of the above-mentioned parameters were consistent in animals from withdrawal experiment, both total and conjugated bilirubin levels were significantly increased after 21 days of BLCO-treatment withdrawal. Taken together, BLCO-induced hepatotoxicity could be due to increased oxidative stress which was not reversible upon withdrawal of treatment within the time course of investigation in male rats.Item Induction of oxidative stress in liver and kidney of rats exposed to Nigerian bonny light crude oil(Wiley Periodicals, Inc., 2010) Adedara, I. A.; Teberen, R.; Ebokaiwe, A. P; Ehwerhemuepha, T.; Farombi, E. O.The local population of Niger-Delta in the Southern part of Nigeria have used bonny light crude oil (BLCO) as a remedy for various ailments and are exposed to some extent to this widespread environmental contaminant or its metabolites through the food chain. BLCO’s hepatorenal toxicity was studied using oxidative stress indices to elucidate the precise nature and mechanism of action. BLCO was orally administered at concentrations of 0, 200, 400, and 800 mg kg21 to adult male rats for 7 days. After exposure, kidney weight was unaffected, but liver weight decreased significantly at 800 mg kg21 only compared with control. BLCO exposure resulted in dose-dependent elevation of serum aminotransferases, total bilirubin, urea, and creatinine. Activities of superoxide dismutase and catalase decreased significantly, whereas c-glutamyltransferase activity and the level of glutathione increased significantly in BLCO-treated animals compared with control in both liver and kidney of rat. Renal activities of glucose-6- phosphatase and 50-nucleotidase markedly decreased in a dose-dependent manner in BLCO-exposed rats. In addition, the levels of hydrogen peroxide and lipid peroxidation significantly increased, dose dependently, in liver and kidney of BLCO-treated rats compared with control. BLCO-treated rats showed marked degeneration of kidney evident in cortical hemorrhages, tubular necrosis, protein casts, and cellular infiltration. However, no treatment-related liver histopathology was observed. The results suggested that BLCO elicits disruption of antioxidant status and concomitant elevation of hydrogen peroxide and lipid peroxidation differentially in liver and kidney of rats. The hepatorenal toxicity of BLCO could be due to induction of oxidative stress in liver and kidney.