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Effect of homocysteine, folates, and cobalamin on endothelial cell- and copper-induced LDL oxidation
Ana María Ronco1, Argelia Garrido, Miguel N Llanos
1Instituto de Nutrición y Tecnología de los Alimentos, Universidad de Chile, Casilla 138-11, Santiago, Chile. amronco@inta.cl
Insights
5-methyltetrahydrofolic acid and vitamin B-12 protect against LDL oxidation, a key factor in atherosclerosis. Folic acid showed no protective effect in this study on LDL oxidative modifications.
Area of Science:
- Biochemistry
- Cardiovascular Science
- Nutritional Science
Background:
- Oxidation of low-density lipoprotein (LDL) is implicated in endothelial dysfunction and atherosclerosis.
- Hyperhomocysteinemia is a condition linked to increased LDL oxidation, which can be improved by folic acid treatment.
- Understanding the role of vitamins in mitigating LDL oxidation is crucial for cardiovascular health.
Purpose of the Study:
- To investigate the effects of folic acid, 5-methyltetrahydrofolic acid, and vitamin B-12 on LDL oxidation.
- To evaluate these vitamins' efficacy in both endothelial cell-catalyzed and cell-free oxidation systems.
- To determine if the presence of homocysteine influences the vitamins' protective effects against LDL oxidation.
Main Methods:
- Utilized two in vitro systems: endothelial cell-catalyzed LDL oxidation and copper-initiated cell-free LDL oxidation.
- Monitored the kinetics of copper-catalyzed LDL oxidation by measuring conjugated diene production.
- Assessed thiobarbituric acid reactive substances (TBARS) production as a marker of lipid peroxidation.
Main Results:
- 5-methyltetrahydrofolic acid demonstrated a concentration-dependent decrease in TBARS production in both systems, irrespective of homocysteine.
- Vitamin B-12 and 5-methyltetrahydrofolic acid significantly increased the lag time of conjugated diene production in the copper-induced system.
- Folic acid exhibited no antioxidant properties in either of the tested in vitro systems.
Conclusions:
- 5-methyltetrahydrofolic acid and vitamin B-12 possess significant antioxidant properties, offering protection against LDL oxidative modifications.
- These findings highlight the potential of 5-methyltetrahydrofolic acid and vitamin B-12 as therapeutic agents against processes contributing to atherosclerosis.
- Folic acid was found to be ineffective in preventing LDL oxidation in the studied in vitro models.
Abstract:
Oxidation of LDL contributes to endothelial dysfunction and atherosclerosis. This process could be associated with hyperhomocysteinemia, a condition that can be reduced after folic acid treatment. Because a reduction in LDL oxidation may improve endothelial function, we studied the effect of some vitamins (folic acid, 5-methyltetrahydrofolic acid, and vitamin B-12) on LDL oxidation, either in the presence or absence of homocysteine. For this purpose, two in vitro systems were used: an endothelial cell-catalyzed LDL oxidation system and a cell-free copper-initiated LDL oxidation system. The kinetics of copper-catalyzed LDL oxidation was determined by continuous monitoring of the production of conjugated dienes in the reaction medium. TBARS production, a parameter of lipid peroxidation, was also evaluated. In both in vitro systems, only 5-methyltetrahydrofolic acid was able to decrease TBARS production in a concentration-dependent manner, independently of the presence or absence of homocysteine. In the copper-induced LDL oxidation system, vitamin B-12 and 5-methyltetrahydrofolic acid increased the lag time of conjugated diene production by 25 and 47%, respectively, suggesting that both vitamins in this system had antioxidant properties. Folic acid was unable to show antioxidant properties when included in either in vitro system. The results demonstrate that 5-methyltetrahydrofolic acid and vitamin B-12 are important protective agents against LDL oxidative modifications.
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