Drug Metabolism and Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan, Nigeria.
Environ Toxicol. 2012 May;27(6):372-9. doi: 10.1002/tox.20660. Epub 2011 Feb 9.
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 kg⁻¹ to adult male rats for 7 days. After exposure, kidney weight was unaffected, but liver weight decreased significantly at 800 mg kg⁻¹ 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 γ-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 5'-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.
尼日利亚南部尼日尔三角洲地区的当地居民曾将邦尼轻质原油 (BLCO) 用作治疗各种疾病的药物，并且在某种程度上通过食物链接触到这种广泛存在的环境污染物或其代谢物。本研究采用氧化应激指标研究 BLCO 的肝肾功能毒性，以阐明其确切的作用机制。BLCO 以 0、200、400 和 800mg/kg 的浓度经口给予成年雄性大鼠，连续 7 天。暴露后，与对照组相比，仅 800mg/kg 组的肾脏重量无变化，但肝脏重量显著下降。BLCO 暴露导致血清转氨酶、总胆红素、尿素和肌酐呈剂量依赖性升高。与对照组相比，BLCO 处理组大鼠肝脏和肾脏中超氧化物歧化酶和过氧化氢酶的活性显著降低，而 γ-谷氨酰转移酶的活性和谷胱甘肽的水平显著升高。BLCO 暴露的大鼠肾脏的葡萄糖-6-磷酸酶和 5'-核苷酸酶的活性呈剂量依赖性显著降低。此外，BLCO 处理大鼠肝脏和肾脏中的过氧化氢和脂质过氧化水平显著升高，呈剂量依赖性。BLCO 处理大鼠的肾脏明显出现皮质出血、肾小管坏死、蛋白管型和细胞浸润等病变。然而，在 BLCO 处理大鼠的肝脏中未观察到与治疗相关的组织病理学变化。这些结果表明，BLCO 会破坏大鼠肝肾功能的抗氧化状态，同时导致肝肾功能中过氧化氢和脂质过氧化水平的差异升高。BLCO 的肝肾功能毒性可能是由于其诱导了肝脏和肾脏中的氧化应激。
