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.
"Thus, the relationship between HCY and observed hsTnT may merely imply the association between the underlying subclinical coronary atherosclerosis and heart failure with minimal myocardial damage. The supplementation of folic acid can be used as an adjuvant therapy in cardiovascular alterations caused by homocysteine.20 "
[Show abstract][Hide abstract] ABSTRACT: Homocysteine (HCY) is associated with an increased risk for cardiovascular disease, possibly leading to myocardial damage. Cardiac troponin T (TnT), a marker of cardiomyocyte injury, can be detected by high-sensitivity TnT (hsTnT) assay. The current study investigated the relationship between plasma HCY and hsTnT levels in a community-based population.
We related plasma levels of hsTnT to HCY levels in 1,497 participants (mean age, 62.4 years; 629 men, 868 women) from a community-based population in Beijing, People's Republic of China.
In multiple logistic regression models, serum HCY was associated with a higher likelihood of detectable hsTnT (odds ratio 1.5; 95% confidence interval 1.07-2.10; P=0.018). A subsequent subgroup analysis found that in subjects aged 65 years and older, the association between hsTnT levels and HCY levels was strengthened. The association between hsTnT and HCY was not present in the younger subgroup (<65 years old).
Levels of serum HCY are associated with hsTnT levels in the elderly, indicating a relationship between HCY and subclinical myocardial damage.
"Oxidant injury has been suggested as a potential mechanism of atherogenesis in hyperhomocysteinemia (Sauls et al., 2007). Results of Kolling et al. (2011) demonstrated that supplementation of folic acid can be used as an adjuvant therapy in cardiovascular alterations caused by Hcy. They observed that Hcy induced oxidative-nitrative stress in a rat heart while folic acid had protective properties. "
[Show abstract][Hide abstract] ABSTRACT: Elevated concentration of homocysteine (Hcy) in human tissues, definied as hyperhomocysteinemia has been correlated with some diseases, such as cardiovascular, neurodegenerative, and kidney disorders. Homocysteine occurs in human blood plasma in several forms, including the most reactive one, the homocysteine thiolactone (HTL) - a cyclic thioester, which represents up to 0.29% of total plasma Hcy. In the article, the effects of hyperhomocysteinemia on the complex process of hemostasis, which regulates the flowing properties of blood, are described. Possible interactions of homocysteine and its different derivatives, including homocysteine thiolactone, with the major components of hemostasis such as endothelial cells, blood platelets, plasmatic fibrinogen and plasminogen, are also discussed. Modifications of hemostatic proteins (N-homocysteinylation or S-homocysteinylation) induced by Hcy or its thiolactone seem to be the main cause of homocysteine biotoxicity in hemostatic abnormalities. It is suggested that Hcy and HTL may also act as oxidants, but various polyphenolic antioxidants are able to inhibit the oxidative damage induced by Hcy or HTL. We also discuss the role of phenolic antioxidants in hyperhomocysteinemia -induced changes in hemostasis.
[Show abstract][Hide abstract] ABSTRACT: Summary and Conclusions A glioblastoma associated with neoplastic reticulum or endothelial elements in the brain of a twelve year old boy was described. The pathogenetic possibilities strongly supported by experimental evidence were, that a malignant transformation might occur in the vascular elements actively growing in gliomas and that two different types of cells — one mesenchymal, the other ectodermal — might undergo malignant degeneration simultaneously under the influence of the same carcinogenic factor.
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