Abstract
Taurine (2-aminoethanesulfonic acid) is found in very high concentrations in mammalian heart1. There has been numerous studies indicating that taurine administration attenuates the degree of myocardial injury commonly associated with various models of heart failure2–5. It has been proposed that the mechanism underlying the cardioprotective activity of taurine relates to its prevention of myocardial calcium overload. The means by which taurine modulates calcium, however, has not been elucidated. One theory which has been proposed as a unifying hypothesis of taurine action, suggests that the effects of taurine are mediated through its interaction with membrane phospholipids. Structurally and chemically many similarities exist between taurine and the head groups of the neutral phospholipids, such as phosphatidylethanolamine and phosphatidylcholine7. In addition, a fairly linear relationship has been found between the ratio of phosphatidylethanolamine/ phosphatidylcholine in the synaptosomal P2B fraction of developing rat brain and taurine content8.
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Hamaguchi, T., Azumal, J., Schaffer, S. (1992). Sarcolemmal Actions of Taurine Linked to Altered Phospholipid N-Methylation. In: Lombardini, J.B., Schaffer, S.W., Azuma, J. (eds) Taurine. Advances in Experimental Medicine and Biology, vol 315. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3436-5_14
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DOI: https://doi.org/10.1007/978-1-4615-3436-5_14
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