Assessment of tolerability against oxidative stress based on the inducible capacity of heme oxygenase-1

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Excessive oxidative stress plays an important role in the mechanism of atherosclerosis. Increased revel of reactive oxygen spices (ROS) within vascular endothelium eventually impedes the vasodilative and cytoprotective actions of nitric oxide (NO). Such a condition is considered to be an early, feature of atherosclerosis, and physiologically detectable as a decrease in endothelium dependent Increased intracellular ROS levels are involved in the mechanisms of diabetes and hyperlipidemia, all of which are major of atherosclerosis Therefore, an assessment of "oxidative status" is obviously relevant to clinical medicine. However, most of the currently available clinical tests are just measuring oxidized wastes. Considering that ROS level is determined by the balance between production and elimination, an assessment of the ability to eliminate ROS may be a major determinant of oxidative state and may be useful to assess an individual susceptibility to atherosclerotic diseases. Focusing on heme oxygenase (HO)-1, one of the major stress defense mechanisms, we found that the capacity to upregulate HO-1mRNA is tightly associated with the severity of coronary artery disease. Furthermore, the individual difference in the stress-induced HO-1 levels was determined by HO-1 gene polymorphism. We propose that clinical use of HO-1 expression profile as a measure for tolerability against oxidative stress may be relevant to early diagnosis of atherosclerotic diseases.