Evidence against oxidative stress as mechanism of endothelial dysfunction in methionine loading model

Nightingale, Angus K., James, Philip P., Morris-Thurgood, Jayne, Harrold, Fraser, Tong, Richard, Jackson, Simon K., Cockcroft, John R. and Frenneaux, Michael P. (2001) Evidence against oxidative stress as mechanism of endothelial dysfunction in methionine loading model. American Journal of Physiology - Heart and Circulatory Physiology, 280 (3). H1334-H1339. ISSN 0363-6135

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Abstract

Endothelial dysfunction reflects reduced nitric oxide (NO) bioavailability due to either reduced production, inactivation of NO, or reduced smooth muscle responsiveness. Oral methionine loading causes acute endothelial dysfunction in healthy subjects and provides a model in which to study mechanisms. Endothelial function was assessed using flow-mediated dilatation (FMD) of the brachial artery in humans. Three markers of oxidative stress were measured ex vivo in venous blood. NO responsiveness was assessed in vascular smooth muscle and platelets. Oral methionine loading induced endothelial dysfunction (FMD decreased from 2.8 +/- 0.8 to 0.3 +/- 0.3% with methionine and from 2.8 +/- 0.8 to 1.3 +/- 0.3% with placebo; P

Item Type:	Article
Uncontrolled Keywords:	adolescent,adult,aged,brachial artery,cross-over studies,endothelium, vascular,homocysteine,humans,lipid peroxidation,male,methionine,middle aged,nitrates,oxidative stress,platelet aggregation,prospective studies,signal transduction,thiobarbituric acid reactive substances
Faculty \ School:	Faculty of Medicine and Health Sciences > Norwich Medical School
UEA Research Groups:	Faculty of Medicine and Health Sciences > Research Groups > Cardiovascular and Metabolic Health
Depositing User:	Pure Connector
Date Deposited:	09 Mar 2015 07:29
Last Modified:	23 Apr 2023 00:59
URI:	https://ueaeprints.uea.ac.uk/id/eprint/52425
DOI:	10.1152/ajpheart.2001.280.3.H1334

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