Recent reports indicated that decabrominated
diphenyl ether (BDE-209) and
decabromodiphenyl ethane (DBDPE) exist extensively in the environment. The toxicity of
BDE-209 has been reported in quite a few studies, whereas the data of DBDPE are relatively rare. However, databases regarding cardiovascular toxicities of both
BDE-209 and DBDPE are lacking. In this study, we investigated the vascular/cardiac
trauma induced by DBDPE after oral exposure and compared the results with those of
BDE-209 using rat model. Male rats were orally administered with
corn oil containing DBDPE or
BDE-209 (5, 50, 500 mg/kg/day) for 28 days, then oxidative stress, morphological and ultrastructural changes of the heart and abdominal aorta, levels of
creatine kinase (CK) and
lactate dehydrogenase (LDH), inflammatory
cytokines,
endothelin-1 (ET-1), and
intercellular adhesion molecule-1 (ICAM-1) in the serum were monitored. Results showed that
BDE-209 and DBDPE caused heart and abdominal aorta morphological and ultrastructural damage, serum CK and LDH elevation, and
antioxidant enzyme activity changes.
BDE-209 and DBDPE-induced
inflammation was characterized by the upregulation of key inflammatory mediators, including
interleukin-1beta (IL-1β),
IL-6,
IL-10, and
tumor necrosis factor alpha (TNFα). Additionally,
BDE-209 and DBDPE led to endothelial dysfunction, as evidenced by the ET-1 and
ICAM-1 elevation. Our findings demonstrated that
BDE-209 and DBDPE could induce oxidative stress,
inflammation, and eventually lead to endothelial dysfunction and cardiovascular injury. Compared to DBDPE, these toxic responses were stronger in the hearts and abdominal aorta of Sprague-Dawley rats exposed to
BDE-209. Our findings indicated a potential deleterious effect of
BDE-209 and DBDPE on the cardiovascular system.