The Effects of Bisphenol A Exposure at Different Developmental Time Points in an Androgen-Sensitive Neuromuscular System in Male Rats

• Published in: Endocrinology (Philadelphia) Vol. 157; no. 8; pp. 2972 - 2977
• Main Authors: Jones, Bryan A, Wagner, Lydia S, Watson, Neil V
• Format: Journal Article
• Language: English
• Published: United States Endocrine Society 01.08.2016
• Subjects: Androgens - pharmacology; Animals; Benzhydryl Compounds - pharmacology; Embryonic Development - drug effects; Endocrine Disruptors - pharmacology; Female; Growth and Development - drug effects; Male; Motor Neurons - drug effects; Motor Neurons - physiology; Phenols - pharmacology; Pregnancy; Prenatal Exposure Delayed Effects - physiopathology; Rats; Rats, Long-Evans; Time Factors
• ISSN: 0013-7227; 1945-7170
• DOI: 10.1210/en.2015-1574

The industrial plasticizer bisphenol A (BPA) is a ubiquitous endocrine disruptor to which the general human population is routinely exposed. Although BPA is well known as an estrogenic mimic, there have been some suggestions that this compound may also alter activity at the androgen receptor. To determine whether BPA does have antiandrogenic properties, we evaluated BPA effects in the spinal nucleus of the bulbocavernosus and dorsolateral nucleus, sexually dimorphic groups of motor neurons in the lumbar spinal cord that are critically dependent on androgens for survival and maintenance, as well as the monomorphic retrodorsolateral nucleus. In experiment 1, we administered varying concentrations of BPA to juvenile rats pre- and postnatally and examined both the number and size of motor neurons in adulthood. In experiment 2, different doses of BPA were given to adult rats for 28 days, after which the soma size of motor neurons were measured. Although no effect of BPA on neural survival or soma size was noted after perinatal BPA exposure, BPA exposure did result in a decrease in soma size in all motor neuron pools after chronic exposure in adulthood. These findings are discussed with regard to putative antiandrogenic effects of BPA; we argue that BPA is not antiandrogenic but is acting through nonandrogen receptor-dependent mechanisms.