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

• Published in: Journal of Toxicology and Environmental Health, Part A Vol. 75; no. 16-17; pp. 948 - 959
• Main Authors: dos Santos, Roger Lyrio, Podratz, Priscila Lang, Sena, Gabriela Cavati, Filho, Vicente Sathler Delgado, Lopes, Pedro Francisco Iguatemy, Gonçalves, Washington Luiz Silva, Alves, Leandro Miranda, Samoto, Vivian Yochiko, Takiya, Christina Maeda, de Castro Miguel, Emilio, Moysés, Margareth Ribeiro, Graceli, Jones Bernardes
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis Group 15.08.2012
• Subjects: Animals; Coronary Vessels - drug effects; Coronary Vessels - physiology; Drug Interactions; Endothelium, Vascular - drug effects; Endothelium, Vascular - ultrastructure; Environmental Pollutants - toxicity; Estradiol - administration & dosage; Estradiol - pharmacokinetics; Female; Rats; Rats, Wistar; Trialkyltin Compounds - toxicity; Vasodilation - drug effects
• ISSN: 1528-7394; 1087-2620
• DOI: 10.1080/15287394.2012.695231

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, 17 β -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 17 β -estradiol. In addition, TBT markedly decreased serum 17 β -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.