| Literature DB >> 23969005 |
Liang Zhou1, Matthew C Beattie, Chieh-Yin Lin, June Liu, Kassim Traore, Vassilios Papadopoulos, Barry R Zirkin, Haolin Chen.
Abstract
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.Entities:
Keywords: 22-hydroxycholesterol; 22HC; 2′,7′-dichlorodihydrofluorescein diacetate; 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide; BSO; DCF; DEHP; GSH; Gsα; IBMX; LH; Leydig cell; MEHP; MTT; Oxidative stress; P5; Phthalate; ROS; STAR; Steroidogenesis; dbcAMP; di-(2-ethylhexyl) phthalate; dibutyryl cAMP; glutathione; isobutyl-methylxanthine; l-buthionine-sulfoximine; luteinizing hormone; mono-(2-ethylhexyl) phthalate; pregnenolone; reactive oxygen species; steroidogenic acute regulatory protein; stimulatory G protein α subunit
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Year: 2013 PMID: 23969005 PMCID: PMC3836854 DOI: 10.1016/j.reprotox.2013.07.025
Source DB: PubMed Journal: Reprod Toxicol ISSN: 0890-6238 Impact factor: 3.143