Taurine has been shown to have potent anti-oxidant properties under various pathophysiological conditions. We reported previously a cellular dysfunction and mitochondrial damage in cardiac myocytes of methionine sulfoxide reductase A (MsrA) gene knockout mice (MsrA(-/-)). In the present study, we have explored the protective effects of taurine against oxidative stress in the heart of MsrA(-/-) mice with or without taurine treatment. Cardiac cell contractility and Ca(2+) dynamics were measured using cell-based assays and in vivo cardiac function was monitored using high-resolution echocardiography in the tested animals. Our data have shown that MsrA(-/-) mice exhibited a progressive cardiac dysfunction with a significant decrease of ejection fraction (EF) and fraction shortening (FS) at age of 8 months compared to the wild type controls at the same age. However, the dysfunction was corrected in MsrA(-/-) mice treated with taurine supplement in the diet for 5 months. We further investigated the cellular mechanism underlying the protective effect of taurine in the heart. Our data indicated that cardiac myocytes from MsrA(-/-) mice treated with taurine exhibited an improved cell contraction and could tolerate oxidative stress better. Furthermore, taurine treatment reduced significantly the protein oxidation levels in mitochondria of MsrA(-/-) hearts, suggesting an anti-oxidant effect of taurine in cardiac mitochondria. Our study demonstrates that long-term treatment of taurine as a diet supplement is beneficial to a heart that is vulnerable to environmental oxidative stresses.
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