PUMA
Istituto di Fisiologia Clinica     
Caruso R., Campolo J., Sedda V., De Chiara B., Della Noce C., Baudo F., Tonini A., Parolini M., Cighetti G., Parodi O. Effect of homocysteine lowering by 5-methyltetrahydrofolate on redox status in hyperhomocysteinemia. In: Journal of Cardiovascular Pharmacology, vol. 47 pp. 549 - 555. Lippincott Williams & Wilkins, 2006.
 
 
Abstract
(English)
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, independent of Hcy lowering. The aim of the study was to assess whether 5-MTHFaffects 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 glutathione (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 in reduced cysteinylglycine (P=0.001). The effects of treatment on Hcy lowering and GSH metabolism were greater in medium than in moderate hyperhomocysteinemia. In conclusion, high-dose 5-MTHF treatment for 3 months ensures marked Hcy lowering to 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.
Subject Homocysteine
Glutathione
Folate


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