Research Paper Volume 11, Issue 8 pp 2241—2252
Exposure to aristolochic acid I compromises the maturational competency of porcine oocytes via oxidative stress-induced DNA damage
- 1 College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China
- 2 Research Center of Combine Traditional Chinese and Western Medicine, Affiliated Traditional Medicine Hospital, Southwest Medical University, Luzhou, Sichuan 646000, China
Received: January 3, 2019 Accepted: April 5, 2019 Published: April 19, 2019https://doi.org/10.18632/aging.101911
How to Cite
Copyright: Zhang et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Aristolochic acid (AA) is a class of carcinogenic and nephrotoxic nitrophenanthrene carboxylic acids naturally found in Aristolochia plants. These plants have been widely used as herbal medicines and also enter the human food chain as the persistent soil pollutants. It has been known that AA exposure is implicated in multiple cancer types, kidney failure and ovarian dysfunction. However, whether AA exposure would influence the oocyte quality has not yet determined. Here, we document that AAI has the negative effects on the competency of oocyte maturation and fertilization. We show that AAI exposure leads to the oocyte meiotic failure via impairing the meiotic apparatus, displaying a prominently defective spindle assembly, actin dynamics and mitochondrial integrity. AAI exposure also causes the abnormal distribution of cortical granules and ovastacin, which is consistent with the observation that fewer sperm bound to the zona pellucida surrounding the unfertilized AAI-exposed eggs, contributing to the fertilization failure. In addition, AAI exposure induces the increased levels of ROS, DNA damage and early apoptosis in porcine oocytes. Collectively, we demonstrate that AAI exposure perturbs the oocyte meiotic progression and fertilization capacity via disruption of both nuclear maturation and cytoplasmic maturation of oocyte, which might be caused by the excessive oxidative stress-induced DNA damage and apoptosis.