Department of Biochemistry and Molecular Biology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, United States.
Reprod Toxicol. 2013 Dec;42:95-101. doi: 10.1016/j.reprotox.2013.07.025. Epub 2013 Aug 19.
Previous studies have shown that phthalate exposure can suppress steroidogenesis. However, the affected components of the steroidogenic pathway, and the mechanisms involved, remain uncertain. We show that incubating MA-10 Leydig cells with mono-(2-ethylhexyl) phthalate (MEHP) resulted in reductions in luteinizing hormone (LH)-stimulated cAMP and progesterone productions. cAMP did not decrease in response to MEHP when the cells were incubated with cholera toxin or forskolin. Incubation of MEHP-treated cells with dibutyryl-cAMP, 22-hydroxycholesterol or pregnenolone inhibited the reductions in progesterone. Increased levels of reactive oxygen species (ROS) occurred in response to MEHP. In cells in which intracellular glutathione was depleted by buthionine sulfoximine pretreatment, the increases in ROS and decreases in progesterone in response to MEHP treatment were exacerbated. These results indicate that MEHP inhibits MA-10 Leydig cell steroidogenesis by targeting LH-stimulated cAMP production and cholesterol transport, and that a likely mechanism by which MEHP acts is through increased oxidative stress.
先前的研究表明邻苯二甲酸酯暴露会抑制类固醇生成。然而,类固醇生成途径中受影响的成分以及涉及的机制仍不确定。我们发现,用邻苯二甲酸二(2-乙基己基)酯(MEHP)孵育 MA-10 间质细胞会导致黄体生成素(LH)刺激的 cAMP 和孕酮产生减少。当细胞用霍乱毒素或 forskolin 孵育时,cAMP 不会因 MEHP 而减少。用二丁酰基 cAMP、22-羟胆固醇或孕烯醇酮孵育 MEHP 处理的细胞可抑制孕酮的减少。MEHP 会引起活性氧(ROS)水平升高。在用丁硫氨酸亚砜预处理耗尽细胞内谷胱甘肽后,MEHP 处理引起的 ROS 增加和孕酮减少加剧。这些结果表明,MEHP 通过靶向 LH 刺激的 cAMP 产生和胆固醇转运来抑制 MA-10 间质细胞的类固醇生成,MEHP 作用的一个可能机制是通过增加氧化应激。