Hyperhomocysteinemia is a risk factor for
cardiovascular disease,
stroke, and
thrombosis; however, the mechanisms by which
homocysteine triggers these dysfunctions are not fully understood. In the present study, we investigated the effect of chronic
hyperhomocysteinemia on some parameters of oxidative stress, namely
thiobarbituric acid reactive substances, an index of lipid peroxidation,
2',7'-dichlorofluorescein (H(2)DCF) oxidation, activities of
antioxidant enzymes named
superoxide dismutase and
catalase, as well as
nitrite levels in heart of young rats. We also evaluated the effect of
folic acid on biochemical alterations elicited by
hyperhomocysteinemia. Wistar rats received daily
subcutaneous injection of
homocysteine (0.3-0.6 μmol/g
body weight) and/or
folic acid (0.011 μmol/g
body weight) from their 6th to the 28th day of life. Controls and treated rats were killed 1 h and/or 12 h after the last injection. Results showed that chronic
homocysteine administration increases lipid peroxidation and reactive species production and decreases enzymatic
antioxidant defenses and
nitrite levels in the heart of young rats killed 1 h, but not 12 h after the last injection of
homocysteine.
Folic acid concurrent administration prevented
homocysteine effects probable by its
antioxidant properties. Our data indicate that oxidative stress is elicited by chronic hyperhomocystenemia, a mechanism that may contribute, at least in part, to the cardiovascular alterations characteristic of hyperhomocysteinemic patients. If confirmed in human beings, our results could propose that the supplementation of
folic acid can be used as an adjuvant
therapy in cardiovascular alterations caused by
homocysteine.