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Role of NAD(P)H oxidase in the cardiovascular effects induced by chronic ethanol consumption.

Grant number: 12/01147-2
Support type:Scholarships in Brazil - Doctorate
Effective date (Start): July 01, 2012
Effective date (End): August 31, 2015
Field of knowledge:Biological Sciences - Pharmacology - Cardiorenal Pharmacology
Principal researcher:Carlos Renato Tirapelli
Grantee:Katia Colombo Marchi
Home Institution: Escola de Enfermagem de Ribeirão Preto (EERP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

Chronic ethanol consumption causes significant changes in cardiac and circulatory functions, appearing as an important risk factor for developing cardiovascular diseases such as hypertension. The first step for the ethanol-associated cardiovascular dysfunction involves the formation of reactive oxygen species (ROS) and reduced bioavailability of nitric oxide (NO), this process being mediated by the enzyme NAD(P)H oxidase. The pathophysiological importance of NAD (P) H oxidase has led many investigators in a large number of experiments both in vivo and in vitro, to the use of inhibitors of this enzyme. Apocynin is considered the main NAD(P)H inhibitor and it displays a powerful anti-inflammatory and anti-oxidizing in a variety of cell and animal models. Currently it is known that there is a family of NAD(P)H oxidases based on the discovery of homologues of gp91phox (also called NOX2). The new homologues, together with gp91phox, are designated as the NOX family of NAP(P)H oxidases and comprise: Nox1, NOX2 (gp91phox), NOX3, Nox4, Nox5 and Duox1 and Duox2. Besides inducing endothelial dysfunction, the ROS produced by NAD(P)H act as signaling molecules and activate intracellular pathways such as MAPKs (Mitogen-Activated Protein Kinase) that play an important role in intracellular signaling and vascular pathophysiology. Ethanol activates the MAPKs, but this process seems to occur indirectly. The hypothesis of this study is that chronic ethanol consumption induces the production of ROS in the cardiovascular system via NAD(P)H oxidase. This process would lead to changes in vascular reactivity, reduced bioavailability of NO, activation of MAPKs and increased blood pressure. Therefore, the aim of this study is to evaluate the involvement of NAD(P)H oxidase in the cardiovascular effects induced by chronic ethanol consumption.

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
MARCHI, KATIA COLOMBO; CERON, CARLA SPERONI; MUNIZ, JAQUELINE J.; DE MARTINIS, BRUNO S.; TANUS-SANTOS, JOSE E.; TIRAPELLI, CARLOS RENATO. NADPH Oxidase Plays a Role on Ethanol-Induced Hypertension and Reactive Oxygen Species Generation in the Vasculature. ALCOHOL AND ALCOHOLISM, v. 51, n. 5, p. 522-534, . (12/01147-2, 13/15824-9)
Academic Publications
(References retrieved automatically from State of São Paulo Research Institutions)
MARCHI, Katia Colombo. Role of NADPH oxidase in increased blood pressure induced by chronic ethanol consumption: evaluation of vascular oxidative stress. 2015. Doctoral Thesis - Universidade de São Paulo (USP). Faculdade de Medicina de Ribeirão Preto (PCARP/BC) Ribeirão Preto.

Please report errors in scientific publications list by writing to: cdi@fapesp.br.