Taurine Cytoprotection: From Cell To System

Abstract

Taurine affects the two major causes of cellular toxicity, causes of cellular toxicity, namely, Ca²⁺ overload and oxidative stress. Often, the beneficial effects of taurine have been attributed to both an improvement in oxidative stress and Ca²⁺ overload. Nonetheless, it is important to recognize that taurine does not directly scavenge superoxide, hydrogen peroxide and superoxide although it directly scavengers HOCl in the presence of myeloperoxidase. Four mechanisms may contribute to taurine-mediated reductions in oxidative stress. First, there is some evidence that taurine might upregulate the antioxidant defenses. Second, N-chlorotaurine suppresses the activity of the neutrophils, thereby reducing their ability to generate free radicals. Third, taurine may prevent Ca²⁺ overload, thereby minimizing free radical generation. Fourth, the major cause of taurine-mediated cytoprotection against certain xenobiotics is the formation of a taurine conjugate that is incapable of generating free radicals. At least three mechanisms contribute to the modulation of Ca²⁺ movement by taurine. First, taurine indirectly alters the activity of the Na⁺/Ca²⁺ exchanger. Second, as an osmolyte, taurine affects the activity of a number of key osmotically sensitive ion transporters. These transporters directly affect Na⁺ and K⁺ transport, which in turn alter Ca²⁺ transport. Third, taurine detoxifies specific xenobiotics that alter Ca²⁺ movement. Taurine displays both short- and long-term cytoprotective activities. Growth retardation, organ damage, and abnormal cardiovascular and renal function have been detected in adult animals that were made taurine deficient in early life. Whether these effects are also found in the human requires further investigation.