Year: 2007
Type: dissertation
Abstract: Hyperhomocysteiuemia or an elevation of blood homocysteine (Hcy) levels is a risk factor for' cardiovascula¡ disot'ders.In this study, the NADPH oxidase involvenrent in Hcy-induced superoxide anion accumulation in the aorta, rvhich led to endothelial dysfunction duling hlperhornocysteinernia was investigated.Hyperhornocysteinemia rvas induced in rats fed a high-metlúonile diet.The NADPH oxidase activity, the levels of superoxide, peroxynitrite and expression of NADPH oxidase p22phox subunit were markedly increased as well as the impaimrent of endothelium-dependent relaxation in aortas isoiated from hyperliomocysteinemic ¡ats.Adrrinist¡ation of an NADPH oxidase inhibitor, apocyrin was able to reverse those effects.Transfection of human vascular cells with p22Pho* siRNA i¡hibited the NADPH oxidase dependent Hcy-induced superoxide anion production.In conclusion, Hcy-stimulated superoxide anion productionin the vascular wail is mediated through the activation of NADPH oxidase, which leads to endothelial dysfunction during hyperhornocysteinernia.
Source: Mspace (University of Manitoba)
Author: Vathsala E.R. Edirimanne
Language: English
Subfield: Physiology (medical)
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2790515849