Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, China.
Regul Toxicol Pharmacol. 2013 Aug;66(3):279-85. doi: 10.1016/j.yrtph.2013.04.005. Epub 2013 Apr 26.
3-methyl-2-quinoxalin benzenevinylketo-1, 4-dioxide (Quinocetone, QCT) is a newly used veterinary drug which has been proven to promote feed efficiency and growth of animals; however, its potential toxicity can't be ignored. Therefore, the present study was aimed to investigate the nephrotoxicity of QCT and the oxidative stress induced by it. Sprague-Dawley rats (SD rats) were randomly divided into four groups with doses of 2400, 800, 50 and 0mg/kg/day with administration of QCT for 4 weeks. Results proved that QCT could induce nephrotoxicity and this phenomenon had dose dependent manner. Simultaneously, this phenomenon was accompanied by intracellular reactive oxygen species (ROS) accumulation, enhanced lipid peroxidation and inhibited antioxidant system, i.e. glutathione S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GSH). Additionally, the higher expression of Nrf2 in QCT treated groups illustrated that QCT-induced oxidative stress would be partly mitigated by the induction of phase II detoxifying enzymes via increasing Nrf2 expression.
3-甲基-2-喹喔啉苯乙烯基酮-1,4-二氧化物（喹乙醇，QCT）是一种新的兽用药物，已被证明能促进动物的饲料效率和生长；然而，其潜在的毒性不容忽视。因此，本研究旨在探讨 QCT 的肾毒性及其诱导的氧化应激。SD 大鼠（SD 大鼠）随机分为四组，剂量分别为 2400、800、50 和 0mg/kg/天，用 QCT 处理 4 周。结果表明，QCT 可诱导肾毒性，且呈剂量依赖性。同时，这种现象伴随着细胞内活性氧（ROS）的积累、脂质过氧化的增强和抗氧化系统的抑制，即谷胱甘肽 S-转移酶（GST）、谷胱甘肽过氧化物酶（GPx）和谷胱甘肽还原酶（GSH）。此外，QCT 处理组中 Nrf2 的高表达表明，QCT 诱导的氧化应激部分可通过增加 Nrf2 表达诱导 II 相解毒酶的产生而得到缓解。
