کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5858804 1562174 2014 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Co-treatment of mouse antral follicles with 17β-estradiol interferes with mono-2-ethylhexyl phthalate (MEHP)-induced atresia and altered apoptosis gene expression
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
Co-treatment of mouse antral follicles with 17β-estradiol interferes with mono-2-ethylhexyl phthalate (MEHP)-induced atresia and altered apoptosis gene expression
چکیده انگلیسی


- MEHP (0.36-36 μM) induces atresia in mouse ovarian antral follicles.
- E2 (1-10 nM) blocks MEHP-induced follicle atresia.
- E2 may block MEHP-induced atresia via changes in Aifm1, Bok, and Bcl2l10 expression.

Mono-2-ethyhexyl phthalate (MEHP) is a metabolite of a plasticizer found in many consumer products. MEHP inhibits mouse ovarian follicle growth by reducing 17β-estradiol (E2) production. Yet, whether MEHP causes follicle death (atresia) is unclear. We hypothesized that MEHP causes atresia by altering apoptosis gene expression, and that E2 co-treatment blocks these effects. Follicles were exposed to MEHP (0.36-36 μM) ± E2 for 48-96 h to determine the effect of MEHP ± E2 on atresia and gene expression. MEHP increased atresia, but this effect was blocked by co-treatment with E2. MEHP increased the expression of the pro-apoptotic gene Aifm1, but decreased that of the pro-apoptotic gene Bok and the anti-apoptotic gene Bcl2l10. E2 interfered with MEHP-induced changes in Aifm1 and Bcl2l10. Our findings suggest that decreased E2 levels are required for MEHP-induced follicle atresia and that Aifm1, Bok, and Bcl2l10 are involved in this process.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Reproductive Toxicology - Volume 45, June 2014, Pages 45-51
نویسندگان
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