Hyperhomocysteinemia alters the cardiac substrate metabolism by impairing NO bioavailability through oxidative stress

Hyperhomocysteinemia (HHCy) has been established as a risk factor for development of cardiovascular disease. Previous studies have focused on the alterations in vascular biology such as vasodilation and white cell infiltration. We have shown that in rats and mice with HHCy, superoxide reduces the ability of NO to regulate mitochondrial function. Molecular mechanisms responsible for HHCy changes in cardiac function and myocardial metabolism are not yet understood. This study was undertaken to determine the global changes in cardiac gene expression in dogs with chronic HHCy using Affymetrix Canine Array. Keywords: Disease state analysis This study was undertaken to determine the global changes in cardiac gene expression in dogs with chronic HHCy using Affymetrix Canine Array. Methionine was added to the drinking water for two weeks. Cardiac RNA was extracted at two weeks from the control and methionine fed groups (n=4).