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Taurine supplements lower oxidative stress and improve heart function in iron-overloaded mice

A study published in the April 20 2004 issue of the journal Circulation reported that administration of the amino acid taurine reduced the cardiovascular effects of iron overload in mice. Secondary iron overload and hereditary hemochromatosis have become recognized as widespread, and are associated with increased mortality from cardiovascular disease. In these conditions, iron is deposited in a variety of tissues, including the heart. Because iron overload is associated with increased free radical production, researchers have endeavored to find therapies that minimize the oxidative damage that occurs. The amino acid taurine is found in high concentrations in the heart muscle, accounting for approximately one-fourth of the free amino acid pool in the human heart. Taurine has potent antioxidant properties and has been found to be associated with dilated cardiomyopathy when deficient.

Researchers from the University of Toronto injected two groups of mice with iron for either four or thirteen weeks to create iron overload, and injected another group with a placebo. Two weeks before receiving the iron the mice received either taurine or a placebo in their drinking water, and were continued on these regimens until the end of the study.

Mice who were injected with iron exhibited signs of heart failure, including peripheral edema, lethargy, and increased mortality. Malondialdehyde and other markers of oxidative stress were increased in the myocardium of this group, and glutathione levels decreased. In iron-overloaded mice who received taurine, mortality was reduced compared to those who did not receive the amino acid. Cardiac function, heart rate and blood pressure were improved in the iron-overloaded mice who received taurine and markers of oxidative stress reduced. Taurine supplements completely prevented the decrease of glutathione that occurred in nonsupplemented iron-overloaded mice. When the hearts of the animals were examined, those who received taurine were found to have reduced myocardial iron levels compared to the mice who received iron without taurine.

The authors conclude that in this mouse model of iron-overload, “taurine supplementation has unequivocal beneficial effects on survival and cardiac structure and function, with marked reductions in iron-induced oxidative stress. Given the impressive benefit and absence of toxicity with taurine supplementation, we propose that increased dietary taurine intake represents an important nutritional modification that may prove to be a useful intervention to reduce the worldwide burden from iron-overload cardiovascular disease.” (Oudit GY et al, “Taurine supplementation reduces oxidative stress and improves cardiovascular function in an iron-overload murine model, Circulation, April 20 2004 p 1877-1885.)