Oxidative stress plays a major part in the development of chronic and degenerative diseases such as cancer, arthritis, aging, autoimmune disorders, cardiovascular and neurodegenerative diseases. Cardiovascular disease is the leading cause of death in the United States and Europe and is poised to become the most significant health problem worldwide. Reactive nitrogen species are involved in the regulation of cardiovascular motor tone, modulation of myocardial contractility, control of cell proliferation and inhibition of platelet activation, aggregation, and adhesion. Cellular constituents of our body are altered in oxidative stress conditions, resulting in various disease states. The oxidative stress can be effectively neutralized by enhancing cellular defenses in the form of antioxidants. To understand the mechanism of action of antioxidants, it is necessary to understand the generation of free radicals and their damaging reactions.
Osteoporosis is a major health problem, and the economic costs are expected to rise due to an increase in life expectancy throughout the world. Its major consequence is fractures, and especially hip fractures are associated with institutionalization and increased mortality. Homocysteine is an amino acid intermediate formed during the metabolism of methionine. Homocysteinuria is a rare autosomal recessive biochemical abnormality which causes elevated plasma concentrations of homocysteine and severe occlusive vascular disease. In patients with homocysteinuria, there is an increased prevalence of skeletal deformities, including osteoporosis, which is a primary risk factor for hip fracture. The high prevalence of osteoporosis among patients with homocysteinuria suggests that high levels of plasmatic homocysteine may also increase the risk of fractures. Nutritional factors such as vitamins B12, B6, and folate are cofactors in homocysteine metabolism, and vitamin intakes may inversely affect plasma homocysteine levels.
