Abstract
Neutrophils recruited into the site of inflammation generate a large number of highly reactive oxidants, including hypochlorous acid (HOCl), produced by the myeloperoxidase-catalyzed oxidation of C1 by hydrogen peroxide1. Hypochlorous acid is the major neutrophil microbicidal agent but its excessive production leads to tissue damage. Oxidative tissue damage is thought to be of pathogenic significance in a large number of diseasese.g.atherosclerosis, malignancy and rheumatoid arthritis. Taurine (Tau), a dominant free amino acid present in most mammalian tissues and in the cytosol of phagocytic cells at high (10–20 mM) concentration2, acts as a major trap for HOCl. The reaction of Tau with HOCl forms the long-lived but weaker oxidant taurine chloramine (Tau-Cl) and thus reduces HOCl toxicity. On the other hand, there is growing evidence that Tau-Cl: (i) down-regulates the production of pro-inflammatory mediators by macrophages, neutrophils and other cells engaged in inflammatory response3, (ii) regulates the function of dendritic cells4, and (iii) enhances protein immunogenecity by chlorination5. This implies Tau-Cl to act as an important physiologic immunoregulatory factor maintaining the delicate balance between mounting an effective immune response, and minimizing the destruction of the tissue by the inflammatory cells.
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Kontny, E., Maśliński, W., Marcinkiewicz, J. (2003). Anti-inflammatory Activities of Taurine Chloramine. In: Lombardini, J.B., Schaffer, S.W., Azuma, J. (eds) Taurine 5. Advances in Experimental Medicine and Biology, vol 526. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0077-3_41
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DOI: https://doi.org/10.1007/978-1-4615-0077-3_41
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