首页> 外文期刊>Reproductive toxicology >Gonadotropin regulation of glutathione synthesis in the rat ovary.
【24h】

Gonadotropin regulation of glutathione synthesis in the rat ovary.

机译:促性腺激素调节大鼠卵巢中谷胱甘肽合成。

获取原文
获取原文并翻译 | 示例
           

摘要

Glutathione (GSH), an antioxidant and conjugator of electrophilic toxicants, prevents toxicant-mediated destruction of ovarian follicles and oocytes. Ovarian GSH has previously been shown to change with estrous cycle stage in rats, suggesting that the gonadotropin hormones may regulate ovarian GSH synthesis. The present studies tested the hypotheses that [1] estrous cycle-related changes in ovarian GSH result from cyclic changes in protein and mRNA expression of the rate-limiting enzyme in GSH synthesis, glutamate cysteine ligase (GCL, also called gamma-glutamylcysteine synthetase), and [2] that these changes result from gonadotropin-mediated regulation of GCL subunit expression. In the first experiment, ovaries were harvested from cycling adult female rats on each stage of the estrous cycle. In the second experiment immature female rats were injected with pregnant mare's serum gonadotropin (PMSG) to stimulate follicular development or with vehicle and killed 8, 24, or 48 h later. In both experiments the ovaries were harvested for [1] total GSH assay, [2] Western analysis for GCL catalytic (GCLc) and regulatory (GCLm) subunit protein levels, or [3] Northern analysis for Gclc and Gclm mRNA levels. Ovarian GSH concentrations and Gclc and Gclm mRNA levels, but not GCL subunit protein levels, varied significantly with estrous cycle stage. PMSG administration significantly increased ovarian GSH concentrations 24 and 48 h later. GCLm protein levels increased significantly at 24 h and 48 h following PMSG. GCLc protein levels did not increase significantly following PMSG. Gcl subunit mRNA levels were not significantly increased at any time point by the planned ANOVA; however, an increase in Gelc at 48 h was identified by t-testing. These results support the hypothesis that gonadotropins regulate ovarian GSH synthesis by modulating GCL subunit expression.
机译:谷胱甘肽(GSH)是一种抗氧化剂和亲电子有毒物质的结合剂,可防止有毒物质介导的卵巢卵泡和卵母细胞的破坏。先前已显示卵巢GSH在大鼠的发情周期阶段会发生变化,这提示促性腺激素可能调节卵巢GSH的合成。本研究检验了以下假设:[1]卵巢GSH的发情周期相关变化是由GSH合成,谷氨酸半胱氨酸连接酶(GCL,也称为γ-谷氨酰半胱氨酸合成酶)的蛋白质和mRNA表达的循环变化引起的。和[2],这些变化是由促性腺激素介导的GCL亚基表达调控引起的。在第一个实验中,在发情周期的每个阶段,从骑自行车的成年雌性大鼠中收获卵巢。在第二个实验中,给未成熟的雌性大鼠注射孕母马的血清促性腺激素(PMSG)以刺激卵泡发育或用赋形剂注射,并在8、24或48小时后杀死。在两个实验中,均收集卵巢用于[1]总GSH测定,[2] Western分析以分析GCL催化(GCLc)和调节性(GCLm)亚基蛋白水平,或[3] Northern分析以分析Gclc和Gclm mRNA水平。卵巢的GSH浓度,Gclc和Gclm mRNA水平(而非GCL亚基蛋白水平)随动情周期阶段的变化而显着变化。在24和48小时后,PMSG给药显着增加了卵巢GSH的浓度。 PMSG后24 h和48 h GCLm蛋白水平显着增加。 PMSG后,GCLc蛋白水平没有明显增加。计划的方差分析在任何时间点均未显着增加Gcl亚基mRNA水平;然而,通过t检验发现48小时时Gelc升高。这些结果支持以下假设:促性腺激素通过调节GCL亚基表达来调节卵巢GSH合成。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号