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BIBTEX RIS

Tributyltin Impairs the Coronary Vasodilation Induced by 17β-Estradiol in Isolated Rat Heart

2012; Taylor & Francis; Volume: 75; Issue: 16-17 Linguagem: Inglês

10.1080/15287394.2012.695231

ISSN

1087-2620

Autores

Roger Lyrio dos Santos, Priscila L. Podratz, Gabriela Cavati Sena, Vicente Sathler Delgado Filho, Pedro Francisco Iguatemy Lopes, Washington Luiz Silva Gonçalves, Leandro Miranda‐Alves, Vívian Yochiko Samoto, Christina Maeda Takiya, Emílio de Castro Miguel, Margareth Ribeiro Moysés, Jones Bernardes Graceli,

Tópico(s)

Effects and risks of endocrine disrupting chemicals

Resumo

Triorganotins, such as tributyltin (TBT), are environmental contaminants that are commonly used as antifouling agents for boats. However, TBT is also known to alter mammalian reproductive functions. Although the female sex hormones are primarily involved in the regulation of reproductive functions, 17β-estradiol also protects against cardiovascular diseases, in that this hormone reduces the incidence of coronary artery disease via coronary vasodilation. The aim of this study was to examine the influence of 100 ng/kg TBT administered daily by oral gavage for 15 d on coronary functions in female Wistar rats. Findings were correlated with changes in sex steroids concentrations. Tributyltin significantly increased the baseline coronary perfusion pressure and impaired vasodilation induced by 17β-estradiol. In addition, TBT markedly decreased serum 17β-estradiol levels accompanied by a significant rise in serum progesterone levels. Tributyltin elevated collagen deposition in the heart interstitium and number of mast cells proximate to the cardiac vessels. There was a positive correlation between the increase in coronary perfusion pressure and incidence of cardiac hypertrophy. In addition, TBT induced endothelium denudation (scanning electron microscopy) and accumulation of platelets. Moreover, TBT impaired coronary vascular reactivity to estradiol (at least in part), resulting in endothelial denudation, enhanced collagen deposition and elevated number of mast cells. Taken together, the present results demonstrate that TBT exposure may be a potential risk factor for cardiovascular disorders in rats.

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