The endothelial dysfunction induced by hyperhomocysteinemia can be reversed by 5-methyltetrahydrofolate (5-MTHF), via homocysteine (Hcy) lowering. An additive antioxidant action of 5-MTHF has been suggested to ameliorate endothelial dysfunction through increased nitric oxide production and superoxide radical scavenging, independently of Hcy lowering. The aim of the study was to assess whether 5-MTHF affects the redox state in hyperhomocysteinemia. We examined the effect of 3 months of oral 5-MTHF treatment (15 mg/day) on the redox pattern in 48 hyperhomocysteinemic subjects compared to 24 untreated hyperhomocysteinemic subjects. By analysis of variance with repeated measures in the 72 subjects, 5-MTHF markedly decreased plasma total Hcy (p-tHcy) (P = 0.0001) and blood total GSH (b-tGSH) (P = 0.002). By multivariate linear regression in the treated subjects, p-tHcy changes from baseline to 3 months, adjusted by baseline p-tHcy levels, correlated only with changes of reduced cysteinylglycine (P = 0.001). The effects of treatment on Hcy lowering and GSH metabolism were larger in medium than in moderate hyperhomocysteinemia. In conclusion, high dose 5-MTHF treatment for three months ensures marked Hcy lowering till normal values even in subjects with high Hcy levels, and should be the treatment of choice in medium hyperhomocysteinemia. Furthermore, 5-MTHF shows a favorable interaction with GSH metabolism.
Effect of homocysteine lowering by 5-methyltetrahydrofolate on redox status in hyperhomocysteinemia / R. Caruso, J. Campolo, V. Sedda, B. De Chiara, C. Dellanoce, F. Baudo, A. Tonini, M. Parolini, G. Cighetti, O. Parodi. - In: JOURNAL OF CARDIOVASCULAR PHARMACOLOGY. - ISSN 0160-2446. - 47:4(2006 Apr), pp. 549-555. [10.1097/01.fjc.0000211748.16573.31]
Effect of homocysteine lowering by 5-methyltetrahydrofolate on redox status in hyperhomocysteinemia
V. Sedda;B. De Chiara;G. Cighetti;
2006
Abstract
The endothelial dysfunction induced by hyperhomocysteinemia can be reversed by 5-methyltetrahydrofolate (5-MTHF), via homocysteine (Hcy) lowering. An additive antioxidant action of 5-MTHF has been suggested to ameliorate endothelial dysfunction through increased nitric oxide production and superoxide radical scavenging, independently of Hcy lowering. The aim of the study was to assess whether 5-MTHF affects the redox state in hyperhomocysteinemia. We examined the effect of 3 months of oral 5-MTHF treatment (15 mg/day) on the redox pattern in 48 hyperhomocysteinemic subjects compared to 24 untreated hyperhomocysteinemic subjects. By analysis of variance with repeated measures in the 72 subjects, 5-MTHF markedly decreased plasma total Hcy (p-tHcy) (P = 0.0001) and blood total GSH (b-tGSH) (P = 0.002). By multivariate linear regression in the treated subjects, p-tHcy changes from baseline to 3 months, adjusted by baseline p-tHcy levels, correlated only with changes of reduced cysteinylglycine (P = 0.001). The effects of treatment on Hcy lowering and GSH metabolism were larger in medium than in moderate hyperhomocysteinemia. In conclusion, high dose 5-MTHF treatment for three months ensures marked Hcy lowering till normal values even in subjects with high Hcy levels, and should be the treatment of choice in medium hyperhomocysteinemia. Furthermore, 5-MTHF shows a favorable interaction with GSH metabolism.Pubblicazioni consigliate
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