Blood glutathione as independent marker of lipid peroxidation in heart failure

Abstract

Background Aminothiols have a critical function as intracellular redox buffers and constitute furthermore an important extracellular redox system. Lipid peroxidation is increased in chronic heart failure (CHF), but the contribution of each thiol to oxidative stress in this syndrome has not been evaluated. Aim To assess the correlation between blood and plasma concentrations of aminothiols and lipid peroxidation as marker of oxidative stress in CHF patients. Methods Blood reduced glutathione (GSH), plasma total and reduced cysteine, cysteinylglycine, homocysteine, GSH, α-tocopherol, ascorbic acid, and free malondialdehyde (MDA) were assessed in samples obtained from 26 CHF heart transplant candidates and 26 age- and gender-matched controls with atherosclerotic risk factors and no history of cardiovascular disease. Results are expressed as median and interquartile range (I–III). Results MDA levels were significantly higher in CHF patients than in controls [1.03 (0.56–1.60) μM vs. 0.70 (0.40–0.83) μM, p = 0.006]. Blood reduced GSH concentrations were significantly higher [662 (327–867) μM vs. 416 (248–571) μM, p = 0.016], while α-tocopherol levels were significantly lower [15 (13–19) μM vs. 21 (17–32) μM, p = 0.001] in CHF patients than in controls. By multivariate logistic regression analysis, the only independent predictors of lipid peroxidation, as expressed by MDA levels ≥ 1.00 μM, were increased blood GSH concentrations (OR 1.003 per unit, 95% CI 1.001 to 1.006, p = 0.008), ischemic (OR 20, 95% CI 2.6 to 155, p = 0.004) and non ischemic CHF etiology (OR 11, 95% CI 1.3 to 99, p = 0.026). Conclusions Abnormalities in intracellular GSH cycling are associated to increased lipid peroxidation in CHF.