Egg white-derived peptides prevent cardiovascular disorders induced by mercury in rats: Role of angiotensin-converting enzyme (ACE) and NADPH oxidase

Autor: Francisca Fernandez, Dalton Valentim Vassallo, Giulia Alessandra Wiggers, Marta Miguel, Danize Aparecida Rizzetti, Franck Maciel Peçanha, Angela Martín, Patricia Corrales, Maylla Ronacher Simões
Přispěvatelé: Conselho Nacional de Desenvolvimento Científico e Tecnológico (Brasil), Ministerio de Economía y Competitividad (España), Consejo Superior de Investigaciones Científicas (España)
Rok vydání: 2017
Předmět:
Zdroj: Digital.CSIC. Repositorio Institucional del CSIC
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ISSN: 0378-4274
Popis: The study aimed to investigate the effects of egg white hydrolysate (EWH) on vascular disorders induced by mercury (Hg). For this, male Wistar rats were treated for 60 days: Untreated (saline, i.m.); Mercury (HgCl2, i.m., 1st dose 4.6 μg/kg, subsequent doses 0.07 μg/kg/day); Hydrolysate (EWH, gavage, 1 g/kg/day); Hydrolysate-Mercury. Systolic (SBP) and diastolic (DBP) blood pressure measurement and vascular reactivity experiments in aorta were performed. We analyzed endothelial dependent and independent vasodilator responses and vasoconstrictor response to phenylephrine (Phe) in absence and presence of endothelium, a NOS inhibitor, a NADPH oxidase inhibitor, the superoxide dismutase, a non-selective COX inhibitor, a selective COX-2 inhibitor, an AT-1 receptors blocker. In situ superoxide anion production, SOD-1, NOX-4, p22phox, COX-2 and AT-1 mRNA levels and NOX-1 protein expression were performed in aorta while the determination of angiotensin converting enzyme (ACE) activity was measured in plasma. As results, EWH prevented the increase in SBP and Phe responses and the endothelial dysfunction elicited by Hg, which was related to decreased ACE activity and NOX activation by EWH and, subsequently, alleviated ROS production and improved NO bioavailability in aorta. In conclusion, EWH could be considered as alternative or complementary treatment tools for Hg-induced cardiovascular damage.
This work was supported by the Conselho Nacional de Desenvolvimento Científico e Tecnológico − CNPq [203440/2014-5] and the Ministerio de Economía y Competitividad − MINECO [AGL2012-32387 and CSIC − Intramural201570I028].
Databáze: OpenAIRE