Suppr超能文献

久效磷农药对虹鳟鱼RTG - 2细胞中类固醇生成及类固醇生成酶转录的影响,涉及蛋白激酶A信号通路。

Effects of monocrotophos pesticide on steroidogenesis and transcription of steroidogenic enzymes in rainbow trout RTG-2 cells involving the protein kinase A signal pathway.

作者信息

Wang Zhenyu, Zhang Xiaona, Tian Hua, Wang Wei, Ru Shaoguo

机构信息

Marine Life Science College, Ocean University of China, Qingdao 266003, China.

Marine Life Science College, Ocean University of China, Qingdao 266003, China.

出版信息

Toxicol In Vitro. 2015 Feb;29(1):155-61. doi: 10.1016/j.tiv.2014.10.001. Epub 2014 Oct 12.

Abstract

Monocrotophos (MCP) pesticide, listed as a UNEP Prior Informed Consent chemical, has been proved to exert toxic effects on the reproductive system of teleost fishes by changing the balance of sex steroid hormones. To investigate the effects of MCP on steroidogenesis in vitro, the rainbow trout (Oncorhynchus mykiss) gonadal cell line RTG-2 was exposed to different MCP concentrations for 48 h. The levels of 17 β-estradiol (E(2)) and testosterone in the medium were measured by radioimmunoassay and the expression of steroidogenic acute regulatory protein and cytochrome P450 enzymes CYP11A1, CYP17, and CYP19A was detected by quantitative real-time PCR. The results showed that 1.0 and 10.0 μg/L MCP pesticide induced E(2) levels and promoted steroidogenic enzyme expression. The possible mechanisms of MCP steroidogenic activity were investigated using inhibitors of protein kinase A (PKA) and protein kinase C. The PKA inhibitor H-89 abrogated the 10.0 μg/L MCP-induced transcriptional up-regulation of steroidogenic enzymes, suggesting an involvement of PKA-dependent mechanism in the disruption of steroidogenesis by the MCP pesticide in rainbow trout RTG-2 cells.

摘要

久效磷(MCP)农药被列为联合国环境规划署事先知情同意化学品,已被证明可通过改变性类固醇激素平衡对硬骨鱼类的生殖系统产生毒性作用。为了研究久效磷对体外类固醇生成的影响,将虹鳟(Oncorhynchus mykiss)性腺细胞系RTG-2暴露于不同浓度的久效磷中48小时。通过放射免疫分析法测定培养基中17β-雌二醇(E2)和睾酮的水平,并通过定量实时PCR检测类固醇生成急性调节蛋白和细胞色素P450酶CYP11A1、CYP17和CYP19A的表达。结果表明,1.0和10.0μg/L的久效磷农药可诱导E2水平并促进类固醇生成酶的表达。使用蛋白激酶A(PKA)和蛋白激酶C抑制剂研究了久效磷类固醇生成活性的可能机制。PKA抑制剂H-89消除了10.0μg/L久效磷诱导的类固醇生成酶转录上调,表明PKA依赖性机制参与了久效磷农药对虹鳟RTG-2细胞类固醇生成的破坏。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验