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

Abstract

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.

The Neurochemical Characterization of Parasympathetic Nerve Fibers in the Porcine Uterine Wall Under Physiological Conditions and After Exposure to Bisphenol A (BPA)

“…Given the above, BPA-induced fluctuations in the expression of VAChT as well as changes in the neurochemical characterization of cholinergic nerves observed during the present study may be the result of a direct impact of the toxin on muscles and neuromuscular junctions. Moreover, because the relaxatory effects of BPS have been reported in previous studies (Jones et al 2016 ), it stands to reason that the increase in the number cholinergic nerves noted after BPA administration is rather due to a suppression of acetylcholine release than an increase in the synthesis of this neuromediator.…”

Modeling Environmentally-Induced Motor Neuron Degeneration in Zebrafish

“…There is currently no direct evidence that BPA exposure is involved in ALS pathogenesis, yet motor neuron degeneration caused by environmental stressors may follow similar mechanisms and thus may be representative of sALS pathogenesis. BPA is a well characterized endocrine disruptor to which humans are ubiquitously exposed 34 . It is known to either activate or antagonize many different receptors such as estrogen receptors (ERs) α and β 35 , membrane-bound estrogen receptor GPR30, glucocorticoid receptors and androgen receptors (AR) 34 .…”

“…BPA is a well characterized endocrine disruptor to which humans are ubiquitously exposed 34 . It is known to either activate or antagonize many different receptors such as estrogen receptors (ERs) α and β 35 , membrane-bound estrogen receptor GPR30, glucocorticoid receptors and androgen receptors (AR) 34 . BPA is structurally similar to 17 β -Estradiol (E2), the most prevalent estrogen in humans.…”

Low-Dose Bisphenol A Increases Bile Duct Proliferation in Juvenile Rats: A Possible Evidence for Risk of Liver Cancer in the Exposed Population?

“…Many researches have been undertaken to investigate the toxicity of BPA on juvenile populations and demonstrated potential harmful effects of BPA exposure on neuromuscular system ( Jones et al ., 2016 ), central nerve system and behavior ( Rebuli et al ., 2014 , 2015 ), adipogenicity and energy metabolism ( Rönn et al ., 2013 ), heart ( Ljunggren et al ., 2016 ), immune responses ( Ménard et al ., 2014 ), endocrine system ( Ahmed, 2016 ), the development of reproductive organs ( Delclos et al ., 2014 ) and liver ( Xia et al ., 2014 ). In most of these studies, however, bona fide signs of carcinogenicity could not be shown for low doses of BPA.…”