The objective of this study was to investigate the toxic effects of buprofezin insecticide on Nile tilapia (Oreochromis niloticus). The fish were exposed to buprofezin at 100 mg/L for 28 days. Compared to control, activity of serum transferases and levels of urea and creatinine showed significant increases. Oxidative stress was recorded manifested by elevated levels of malondialdehyde (MDA), reduced concentrations of reduced glutathione (GSH) and inhibition of activities of superoxide dismutase (SOD) and catalase (CAT) in liver and kidney. Examination of peripheral RBCs revealed elevated frequency of micronucleated cell. Interleukin 1 beta (IL‐1β) gene was upregulated in liver, muscle and brain, while that of cyclooxygenase 2 (COX‐2) gene increased in liver and muscle, but not in brain. Histopathological alterations were recorded in liver, kidneys, brain, gills, pancreas, spleen, intestine, muscle and ovaries. The immunohistochemical detection of caspase‐3 in the liver revealed no differences between treated and control groups; however, the expression of inducible nitric oxide synthase (iNOS) was demonstrated in hepatocytes and hepatopancreas in buprofezin‐treated group compared to control. It has been concluded that the tissue damage induced by buprofezin in Nile tilapia is mediated by oxidative stress and inflammatory response but not by apoptosis.

中文翻译：

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丁苯丙酸中毒牵涉尼罗罗非鱼（Oreochromis niloticus）对健康的危害

这项研究的目的是调查丁丙诺啡杀虫剂对尼罗罗非鱼（Oreochromis niloticus）的毒性作用。）。将鱼暴露于100 mg / L的布洛芬锌中28天。与对照组相比，血清转移酶的活性以及尿素和肌酐的水平显着增加。氧化应激表现为丙二醛（MDA）含量升高，还原型谷胱甘肽（GSH）浓度降低以及肝和肾脏中超氧化物歧化酶（SOD）和过氧化氢酶（CAT）活性受到抑制。外周红细胞检查发现微核细胞的频率升高。肝脏，肌肉和大脑中的白介素1 beta（IL-1β）基因上调，而肝脏和肌肉中的环氧合酶2（COX-2）基因则升高，但大脑中没有。在肝，肾，脑，腮，胰腺，脾，肠，肌肉和卵巢中记录了组织病理学改变。肝脏中caspase-3的免疫组织化学检测显示，治疗组和对照组之间没有差异；然而，与对照组相比，丁苯丙酸治疗组的肝细胞和肝胰腺中可诱导型一氧化氮合酶（iNOS）的表达得到证实。已经得出结论，在盐酸尼罗罗非鱼中由布洛芬锌引起的组织损伤是由氧化应激和炎症反应介导的，而不是由细胞凋亡介导的。