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Characterization of Molecular Mechanisms of In vivo UVR Induced Cataract
Published on: November 28, 2012
UV-B filter octylmethoxycinnamate-induced vascular endothelial disruption on rat aorta: In silico and in vitro
Margarida Lorigo1, Elisa Cairrao1
1CICS-UBI, Health Sciences Research Centre, University of Beira Interior, 6200-506, Covilhã, Portugal; FCS - UBI, Faculty of Health Sciences, University of Beira Interior, 6200-506, Covilhã, Portugal; C4-UBI, Cloud Computing Competence Centre, University of Beira Interior, 6200-501, Covilhã, Portugal.
Abstract:
Throughout human life, an extensive and varied range of emerging environmental contaminants, called endocrine disruptors (EDCs), cause adverse health effects, including in the cardiovascular (CV) system. Cardiovascular diseases (CVD) are worryingly one of the leading causes of all mortality and mobility worldwide. The UV-B filter octylmethoxycinnamate (also designated octinoxate, or ethylhexyl methoxycinnamate (CAS number: 5466-77-3)) is an EDC widely present in all personal care products. However, to date, there are no studies evaluating the OMC-induced effects on vasculature using animal models to improve human cardiovascular health. This work analysed the effects of OMC on rat aorta vasculature and explored the modes of action implicated in these effects. Our results indicated that OMC relaxes the rat aorta by endothelium-dependent mechanisms through the signaling pathways of cyclic nucleotides and by endothelium-independent mechanisms involving inhibition of L-Type voltage-operated Ca2+ channels (L-Type VOCC). Overall, OMC toxicity on rat aorta may produce hypotension via vasodilation due to excessive NO release and blockade of L-Type VOCC. Moreover, the OMC-induced endothelial dysfunction may also occur by promoting the endothelial release of endothelin-1. Therefore, our findings demonstrate that exposure to OMC alters the reactivity of the rat aorta and highlight that long-term OMC exposure may increase the risk of human CV diseases.
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