Endocrine Abstracts (2017) 49 EP1100 | DOI: 10.1530/endoabs.49.EP1100

Phthalates induce ovarian failure through disturbance in folliculogenesis and steroidogenesis

Dinh Nam Tran, Jae Hwan Lee, Changhwan Ahn, Jin Yong An, Seon Young Park & Eui-Bae Jeung

Chungbuk National University, Cheongju, Chungbuk, Republic of Korea.

Introduction: Phthalates are chemicals used to improve the plasticity of industrial polymers and used in commercial products such as toys, paints, packaging materials, medicals devices and personal care items. Phthalates, endocrine disrupting chemicals, have been documented to cause adverse effects to the human health such as breast cancer in female, reduced uroogenital distance and changed the expression of steroidogenesis and folliculogenessis. In this study, we investigated the impact of di(2-ethylhexyl) phthalate (DEHP), di-n-butyl phthalate (DBP), and butyl benzyl phthalate (BBP) on loss of ovarian function through folliculogenesis and steroidogenesis. 4-Vinylcyclohexene diepoxide (VCD), a disruptor of ovarian small pre-antral follicles, was used as a positive control.

Methods: Female Spargue-Dawley rats (8 weeks of age, 160–180 g bodyweight) were administered VCD (80 mg/kg) by intraperitoneal, DEHP (25 mg/kg), BBP (250 mg/kg) and DBP (250 mg/kg) by oral gavage in 0.3 ml of corn oil at LOAEL during 6 weeks. Vaginal smear was collected at 9 a.m every day to check estrus cycle. Blood, pituitary, uterine and ovaries were collected after 24 h final injection.

Results: There was significantly increased in body weight of DEHP groups compared to other groups. Estrus cycle in DEHP and DBP groups showed no difference comparing with vehicle group. However, diestrus phase in VCD and BBP groups drew out compared to vehicle group. The transcriptional levels of folliculogenesis-related genes (Foxl2, Kitl and Amh) and steroidogenesis-related genes (Star and Cyp11a1) were changed.

Conclusion: Our findings suggest that these phthalates can induce premature ovarian failure by disturbance in folliculogenesis and steroidogenesis and failure in hormone regulation.

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