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短期暴露于壬基酚会导致成年雌性大鼠胰腺氧化应激,并改变肝脏葡萄糖代谢。

Short-term exposure to nonylphenol induces pancreatic oxidative stress and alters liver glucose metabolism in adult female rats.

机构信息

Department of Biochemistry and Molecular Biology, School of Life Sciences, Pondicherry University, Pondicherry 605 014, India.

出版信息

J Biochem Mol Toxicol. 2011 Mar-Apr;25(2):77-83. doi: 10.1002/jbt.20361.

Abstract

Nonylphenol is known to have estrogenic properties and has been reported to cause health hazards to animals and humans. The effects of nonylphenol on pancreas are not clearly elucidated. In this study, we sought to evaluate the effects of nonylphenol on the oxidative status of pancreas and consequential effects of nonylphenol on some of the end points of carbohydrate metabolism in the female rats. Rats were administered nonylphenol orally at the doses of 1.5, 15, and 150 mg/kg of body weight per day for 7 days. After 24 h of last dosing, the animals were sacrificed by cervical dislocation. The activities of pancreatic superoxide dismutase and catalase were significantly decreased with a concomitant increase in the levels of H2O2 and lipid peroxidation. Nonylphenol increased plasma insulin levels with a concomitant decrease in the levels of plasma glucose as compared to the control groups of rats. A dose-dependent increase in the activities of liver hexokinase and phosphofructokinase was recorded along with decreased activity of glycogen phosphorylase in liver. Western blot analysis revealed a significant decrease in the levels of GLUT-2. These results show that nonylphenol causes oxidative stress in pancreas and impairs liver glucose homeostasis.

摘要

壬基酚具有雌激素特性,据报道会对动物和人类造成健康危害。壬基酚对胰腺的影响尚不清楚。在这项研究中,我们试图评估壬基酚对胰腺氧化状态的影响,以及壬基酚对雌性大鼠碳水化合物代谢某些终点的影响。大鼠每天经口给予 1.5、15 和 150mg/kg 体重的壬基酚,连续 7 天。末次给药 24 小时后,通过颈椎脱位处死动物。胰腺中超氧化物歧化酶和过氧化氢酶的活性显著降低,同时 H2O2 和脂质过氧化水平升高。与对照组大鼠相比,壬基酚使血浆胰岛素水平升高,同时使血浆葡萄糖水平降低。肝己糖激酶和磷酸果糖激酶的活性呈剂量依赖性增加,而肝糖原磷酸化酶的活性降低。Western blot 分析显示 GLUT-2 水平显著降低。这些结果表明,壬基酚导致胰腺氧化应激,并损害肝脏葡萄糖稳态。

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