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Cardiovascular Toxicology

Erschienen in:

01.03.2012

NAD(P)H:Quinone Oxidoreductase 1 and its Potential Protective Role in Cardiovascular Diseases and Related Conditions

verfasst von: Hong Zhu, Yunbo Li

Erschienen in: Cardiovascular Toxicology | Ausgabe 1/2012

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Abstract

NAD(P)H:quinone oxidoreductase (NQO) represents a family of flavoproteins that catalyze the two-electron reduction of quinones and their derivatives. In mammalian systems, there are two members of NQO, namely, NQO1 and NQO2. NQO1 utilizes NAD(P)H, whereas NQO2 employs dihydronicotinamide riboside (NRH) as the electron donors. In addition to the well-documented action in reducing quinone compounds and preventing the formation of reactive oxygen species, NQO enzymes, especially NQO1 also possess other important biological activities. These include anti-inflammatory effects, direct scavenging of superoxide anion radicals, and stabilization of p53 and other tumor suppressors. Recently, multiple studies in animal models demonstrated a potential role for NQO1 in protecting against cardiovascular injury and related conditions, including atherogenesis, dyslipidemia, and insulin resistance. Functional gene polymorphisms have been identified in human NQO1 gene. Studies on the association between NQO1 gene polymorphisms and susceptibility to disease development also suggested a possible involvement of NQO1 in human cardiovascular diseases and metabolic syndrome. This review is intended to summarize the recent development regarding the biochemical properties and molecular regulation of NQO1 and its potential beneficial role in cardiovascular diseases and related conditions, including metabolic syndrome.

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Titel: NAD(P)H:Quinone Oxidoreductase 1 and its Potential Protective Role in Cardiovascular Diseases and Related Conditions
verfasst von: Hong Zhu
Yunbo Li
Publikationsdatum: 01.03.2012
Verlag: Humana Press Inc
Erschienen in: Cardiovascular Toxicology / Ausgabe 1/2012
Print ISSN: 1530-7905
Elektronische ISSN: 1559-0259
DOI: https://doi.org/10.1007/s12012-011-9136-9

Springer Medizin

Abstract

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