The toxic effects and possible mechanisms of Bisphenol A on oocyte maturation of porcine in vitro
PDF | HTML | How to cite
Metrics: PDF 3270 views | HTML 3157 views | ?
Teng Wang1, Jun Han1, Xing Duan1, Bo Xiong1, Xiang-Shun Cui2, Nam-Hyung Kim2, Hong-Lin Liu1, Shao-Chen Sun1
1College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China
2Department of Animal Sciences, Chungbuk National University, Cheongju 361-763, Korea
Shao-Chen Sun, e-mail: [email protected]
Keywords: BPA, cytoskeleton, autophagy/apoptosis, oxidative stress, epigenetics
Received: January 20, 2016 Accepted: March 28, 2016 Published: April 11, 2016
Bisphenol A (BPA) and Di-(2-ethylhexyl) phthalate (DEHP) are widely used in the plastic industry such as water bottles, containers, packaging and toys. BPA and DEHP are shown to be the endocrine disruptors which disturb the endocrine system and are linked to several diseases including infertility. In this study, we investigated the effects of BPA exposure on porcine oocyte maturation and its possible reasons. Our results showed that: (i) the rates of oocyte maturation significantly decreased with 250 μM BPA treatment in vitro, but not DEHP. This might be due to the delayed cell cycle progression of oocyte maturation. (ii) BPA treatment resulted in abnormal cytoskeletons on porcine oocytes, showing with aberrant actin distribution, spindle morphology and chromosome alignment, which was further confirmed by the reduced p-MAPK level. (iii) The fluorescence intensity of histone methylation (H3K4me2) and DNA methylation (5 mC) levels were altered after BPA treatment, indicating that epigenetic modification was disturbed. (iv) BPA-exposed oocytes had higher rates of early stage apoptosis/autophagy, and this may be resulted from the increased level of oxidative stress. Collectively, our results indicated that porcine oocytes maturation was disrupted after BPA treatment through disrupting cytoskeletal dynamics, epigenetic modifications and inducing apoptosis/autophagy.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.