Potential hepatic toxicity of buprofezin at sublethal concentrations: ROS-mediated conversion of energy metabolism
Potential hepatic toxicity of buprofezin at sublethal concentrations: ROS-mediated conversion of energy metabolism
复制标题
亚致死浓度噻嗪酮的潜在肝毒性：ROS介导的能量代谢转化
DOI：
10.1016/j.jhazmat.2016.08.027
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发表时间：
2016-12-15
影响因子：
13.6
通讯作者：
Sang, Nan
中科院分区：
文献类型：
--
作者：
Ji, Xiaotong;Ku, Tingting;Sang, Nan
Buprofezin is known for its broad-spectrum action and environmental safety. The popularity of buprofezin has raised concerns about its potentially adverse effects on human health and risk to the environment. In this study, we first identified the liver as one of the major organs in which buprofezin accumulated, and we detected a severe oxidative stress response. Next, we demonstrated that sublethal concentrations of buprofezin promoted the conversion of energy metabolism from the aerobic tricarboxylic acid (TCA) cycle and oxidative phosphorylation to anaerobic glycolysis. Importantly, reactive oxygen species (ROS) generation partially accounted for the shunting of the energy metabolism through the buprofezin-mediated inhibition of cytochrome c oxidase activity. ROS directly perturbed the activities of several key TCA cycle enzymes, stimulated glycolysis, and indirectly disturbed the activity of the respiratory chain complex by altering mitochondrial DNA (mtDNA). These findings clarify the potential mechanisms of buprofezin toxicity and provide biomarkers for buprofezin-mediated hepatotoxicity at sublethal concentrations. (C) 2016 Elsevier B.V. All rights reserved.
