Prenatal exposure to bisphenol A at the reference dose impairs mitochondria in the heart of neonatal rats

• Published in: Journal of applied toxicology Vol. 34; no. 9; pp. 1012 - 1022
• Main Authors: Jiang, Ying, Liu, Juan, Li, Yuanyuan, Chang, Huailong, Li, Gengqi, Xu, Bing, Chen, Xi, Li, Weiyong, Xia, Wei, Xu, Shunqing
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01.09.2014; Wiley Subscription Services, Inc
• Subjects: Animals; Benzhydryl Compounds - administration & dosage; Bisphenol A; BPA; Cardiovascular disease; Dose-Response Relationship, Drug; Energy Metabolism; Epidemiology; Exposure; Female; Gene Expression; Gestation; Heart; Heart - drug effects; Heart - physiopathology; Heart diseases; Immunohistochemistry; Male; Membrane Potential, Mitochondrial - drug effects; Mitochondria; mitochondria dysfunction; Mitochondria, Heart - drug effects; Mitochondria, Heart - pathology; Phenols - administration & dosage; Pregnancy; prenatal exposure; Prenatal Exposure Delayed Effects - chemically induced; Prenatal Exposure Delayed Effects - physiopathology; Rats; Rats, Wistar; reference dose; RNA, Messenger - genetics; RNA, Messenger - metabolism; Rodents; Succinate Dehydrogenase - metabolism; BPA; prenatal exposure; mitochondria dysfunction; reference dose; heart
• ISSN: 0260-437X; 1099-1263
• DOI: 10.1002/jat.2924

ABSTRACT Bisphenol A (BPA) exposure has been reported to be epidemiologically associated with heart disease. As mitochondria play an important role in the early development of the heart and in the pathogenesis of heart disease, the current study investigated the possibility of cardiac mitochondrial injury in neonatal rat heart prenatally exposed to BPA. Pregnant Wistar rats were exposed to BPA 50 µg kg–1 day–1 or corn oil 1 ml kg–1 by oral gavage throughout gestation. Heart samples from pups on postnatal day 1 were isolated for analysis. Ultrastructure results showed mild swelling with dissociation of cristae in myocardial mitochondria of BPA‐treated rats. Additionally, mitochondrial membrane potential and the activity of respiratory chain complex II were significantly decreased. However, the activities of other three complexes (CI, CIII, CIV) and cardiac histology stayed normal. The expression levels of some key regulators involved in mitochondria energy metabolism and ATP‐generating pathways were downregulated. The study demonstrated for the first time that prenatal exposure to BPA at the reference dose could impair mitochondria in the hearts of neonatal rats. Copyright © 2013 John Wiley & Sons, Ltd. Bisphenol A exposure is epidemiologically associated with heart disease. We found prenatal exposure to BPA at the reference dose induced mild ultrastructure changes in myocardial mitochondria at birth day. Mitochondrial membrane potential and the activity of respiratory chain complex II were significantly decreased. The expression levels of key regulators involved in mitochondria energy metabolism and ATP‐generating pathways were down‐regulated. The study demonstrated that prenatal exposure to BPA at the reference dose could impair mitochondria in the hearts of neonatal rats.