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  • Recently the toxicity of TBT

    2021-11-24

    Recently, the toxicity of TBT was demonstrated at the vascular level in animal models (Nath, 2008), and the results obtained so far suggest that TBT may be a potential risk factor for cardiovascular diseases. TBT is capable to alter the coronary vascular reactivity to estradiol (dos Santos et al., 2012) and also to modify the morphology and functionality of the aortic artery in rodent models (Rodrigues et al., 2014) and also in endothelial buy ink sale of pigs (Bernardini et al., 2016; Botelho et al., 2015). Dos Santos et al. (2012) also demonstrated that TBT impairs the coronary vasodilation induced by 17β-estradiol in rat coronary arteries. The mechanisms that regulate the contractile state of the smooth muscle buy ink sale cells in the human umbilical artery (HUA) are very important for optimum gas and nutrient exchange between the foetus and the placenta. The control of umbilical blood flow depends on vasoactive substances, either released locally or existing in the circulation (Leung et al., 2006; Tufan et al., 2003), such as serotonin (5-hydroxytryptamine; 5-HT) and histamine, since the umbilical cord is not innervated. Moreover, preeclampsia is associated with an increase or decrease in histamine and 5-HT release and with the sensitivity of the HUA to these mediators, which can lead to changes in vascular resistance (Brew and Sullivan, 2006; Feinberg, 2006; Gupta et al., 2006; Ishii et al., 1993; Redman and Sargent, 2005). Thus, 5-HT and histamine can regulate the HUA tonus and are involved in some pathological processes that disturb umbilical circulation.
    Methods
    Results
    Discussion To investigate the long term effects of TBT exposure in the contractility of HUA we incubated HUA rings with 0.1 nM, 0.1 μM and 100 μM of TBT and tested the HUA with 5-HT, histamine and KCl. Subsequently the HUA rings were exposed to the different concentrations of TBT (0.1 nM–100 μM). The range of concentrations used in this study are according to the detected in human liver and blood, that are higher than 300 nM (Antizar-Ladislao, 2008; Kannan et al., 1999), which would allow us to extrapolate the results obtained in this study to those observed in vivo. Moreover, the study of long term effects of TBT is particularly important as this compound is a potent endocrine disrupting chemical and as most of the endocrine disrupting chemicals (EDCs) their effects are a consequence of continuous exposures (Gore et al., 2015). Furthermore, in the last decades, several studies suggested that the continuous exposure to EDCs may be associated with the increase in cardiovascular diseases, one of the main causes of death worldwide (Mariana et al., 2016; Salehi-Abargouei et al., 2013). Previous studies have shown that there are specific receptors involved in the contractile capacity of the three contractile agents used (serotonin, histamine and KCl). It has been demonstrated that in HUA the contractile capacity of 5-HT is associated with the activation of two specific receptors, 5-HT1B/1D and 5-HT2A (Cairrao et al., 2008; Lovren et al., 1999; Santos-Silva, 2009). The 5-HT2A receptor stimulates phospholipase C, increasing the levels of IP3 and 5-HT1B/1D, in turn, is coupled to Gi/Go proteins, which inhibit adenylate cyclase (Cairrao et al., 2008; Santos-Silva, 2009; Steinert et al., 2002; Tufan, 2003 #228). Santos-Silva et al. verified that in the HUA 5-HT1B/1D receptors induce a dual effect because in some of the arteries induced a small contractile effect and in some cases a bigger contraction was observed (Santos-Silva, 2009). The contractile capacity of histamine is related to the activation of the H1 receptor that induces HUA contraction by the activation of phospholipase C, and also the increase of IP3 levels (Cairrao et al., 2008; Hawley et al., 1995; Santos-Silva, 2009). The H2 receptor activation causes an increase in the cAMP intracellular concentration due to the Gs activation, and consequently the HUA relaxation (Cairrao et al., 2008; Santos-Silva, 2009). Regarding the mechanism involved in the contraction by KCl, it is mainly due to the influx of calcium by the voltage-dependent calcium channels (Tufan et al., 2003).