Patlolla Anita K, Kumari S Anitha, Madhusudhanachary P, Turner Timothy, Tchounwou Paul B
NIH-RCMI Center for Environmental Health, College of Science, Engineering and Technology, Jackson State University, Jackson, MS, USA.
Department of Biology, Jackson State University, Jackson, MS, USA.
Curr Top Biochem Res. 2018;19:1-12.
The present study was conducted to evaluate the response of kidneys in Wistar rats following long-term exposure to AlO nanomaterials (NMs). To achieve this objective, AlO of three different sizes (30 nm, 40 nm and bulk) was orally administered for 28 days to 9 groups of 10 Wistar rats each at the dose of 500, 1000 and 2000 mg/kg/rat. A tenth group of 10 rats received distilled water and served as control. After 28 days of exposure the animals were sacrificed and the serum was collected and tested for the activity levels of creatinine and urea following standard methods. Induction of oxidative stress was also investigated by assessing thiobarbituric acid reactive substances (TBARS) (MDA), protein carbonyl, reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) activities. A histopathological evaluation was also performed to determine the extent of kidney damage. The results showed that both serum creatinine and serum urea levels increased significantly in the treated rats compared to control animals. The increase was found to be more in AlO-30 nm treated rats followed by AlO-40 nm and AlO-bulk treated rats in a dose-dependent manner. Further administration of AlO significantly increased the activities of TBARS, protein carbonyl, catalase and decreased the activities of GSH and SOD in a dose-dependent manner in the kidney of rats compared with the control group. Histopathological evaluation showed significant morphological alterations in kidney tissues of treated rats in accordance with biochemical parameters. Taken together, the results of this study demonstrate that AlO is nephrotoxic and its toxicity may be mediated through oxidative stress. Further, the results suggest that prolonged oral exposure to AlO NMs has the potential to cause biochemical and histological alterations in kidney of rats at high concentration.
本研究旨在评估Wistar大鼠长期暴露于AlO纳米材料(NMs)后肾脏的反应。为实现这一目标,将三种不同尺寸(30纳米、40纳米和块状)的AlO以500、1000和2000毫克/千克/大鼠的剂量分别口服给予9组Wistar大鼠,每组10只,持续28天。第十组10只大鼠接受蒸馏水作为对照。暴露28天后,处死动物,收集血清并按照标准方法检测肌酐和尿素的活性水平。还通过评估硫代巴比妥酸反应性物质(TBARS)(丙二醛,MDA)、蛋白质羰基、还原型谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性来研究氧化应激的诱导情况。还进行了组织病理学评估以确定肾脏损伤的程度。结果表明,与对照动物相比,处理组大鼠的血清肌酐和血清尿素水平均显著升高。发现AlO - 30纳米处理组大鼠的升高幅度更大,其次是AlO - 40纳米处理组和AlO块状处理组大鼠,呈剂量依赖性。与对照组相比,进一步给予AlO可使大鼠肾脏中TBARS、蛋白质羰基、过氧化氢酶的活性显著增加,并使GSH和SOD的活性呈剂量依赖性降低。组织病理学评估显示,处理组大鼠肾脏组织的形态学改变与生化参数一致。综上所述,本研究结果表明AlO具有肾毒性,其毒性可能通过氧化应激介导。此外,结果表明长期口服暴露于AlO纳米材料有可能在高浓度下导致大鼠肾脏发生生化和组织学改变。