Corticosteroid Disruption By Chronic BDE-47 Administration Is Associated with Cardiovascular Pathophysiology in Adult Male Rats

Presentation Number: MON 375
Date of Presentation: April 3rd, 2017

Chad D Schupbach and Phillip G Kopf*
Midwestern University, Downers Grove, IL


Polybrominated diphenyl ethers (PBDEs) and their metabolites have been previously shown to alter various endocrine biosynthetic pathways including thyroid hormone, estrogens, and androgens. The adrenal gland is one of the primary endocrine organs in which PBDEs accumulate. Previous work in our laboratory has demonstrated that BDE-47 increases basal and stimulated aldosterone and cortisol secretion in a human adrenocortical cell line. Based on these in vitro data, a chronic study in adult rats was conducted. Sprague Dawley male rats (10 weeks of age) were orally exposed to vehicle (DMSO), 10 µg/kg BDE-47, or 100 µg/kg BDE-47, 5 days per week for 16 weeks. At the end of the study, various organ weights were measured, plasma was collected for corticosteroid analysis, and vascular reactivity of mesenteric resistance arterioles was evaluated. Adrenal weights were significantly increased in both BDE-47 treatment groups (adrenal weight in g/kg body weight, vehicle: 0.0934±0.0038, 10 µg/kg BDE-47: 0.1136±0.0053, 100 µg/kg BDE-47: 0.1175±0.0032, p<0.05). Additionally, heart and left ventricle weights were significantly increased in the 100 µg/kg BDE-47 treatment group (heart weight in g/kg body weight, vehicle: 2.7661±0.0369, 100 µg/kg BDE-47: 3.1301±0.0863, p<0.05)(left ventricle weight in g/kg body weight, vehicle: 2.2049±0.0523, 100 µg/kg BDE-47: 2.5246±0.0656, p<0.05). There were no significant changes in right ventricle, liver, or kidney weights. Plasma corticosterone was significantly elevated in the 100 µg/kg BDE-47 treatment group (corticosterone in ng/mL, vehicle: 69.57±14.61, 100 µg/kg BDE-47: 449.43±73.01, p<0.05). While there was no difference in acetylcholine-induced relaxation in mesenteric arterioles, there was a significant increase in phenylephrine contractions in mesenteric arterioles from both BDE-47 treatment groups. These data indicate that chronic BDE-47 exposure results in elevated production of adrenal corticosteroids and cardiovascular pathophysiology. Blood pressure telemetry studies are underway to determine if BDE-47 exposure results in hypertension. Future studies will determine if the cardiovascular pathophysiology observed is directly caused by the excess corticosteroid production in this model of chronic BDE-47 exposure.


Nothing to Disclose: CDS, PGK