Beneficial Role Of Taurine Supplementation To The Complement System Via Myeloperoxidase In Acute Kidney Failure & Chronic Renal Disease. Mechanisms Involved To Alleviate Pathogenesis

Anthony M. Kyriakopoulos , Stella Balliou  and Vasillis Zoumpourlis 

NASCO AD Biotechnology Laboratory, 11 Sachtouri str., 18536, Pireas, Greece

Biomedical Applications Unit, Institute of Biological Research and Biotechnology, National Hellenic Research Foundation, 48 Vas. Constantinou Ave., 116 35 Athens, Greece


Redox potential governs a plethora of cellular functions specifically related to their proliferative activity towards the organism’s status to health or disease. Taurine metabolism as redox potential regulator is implicated in glutamate biochemical pathways where the γ-glutamyl cycle protagonists, to maintain cysteine constant concentrations and hence health status. This is extremely valuable to maintain normal cellular and protein functions that by taurine are under tight genetic regulation. As taurine primarily and continuously regulate myeloperoxidase activity to avoid oxidative bursts, responsible for brain, cardiac and nephron diseases, amongst others, the supplementation, production and future clinical use of taurine, taurine derivatives and other haloamine oxidants, named as taurine related molecules, TRM, gain clinical significance for their use against kidney disease. The maintenance of myeloperoxidase activity by infiltrating neutrophils at sites of inflammation as well as eosinophile peroxidase and other chemical gradient producing enzymes, has direct medical importance to the impaired complement activity that contributes significantly to kidney pathogenesis. Newer therapies with monoclonal antibodies against specific adhesion molecules related to improper complement activity seem to biochemically benefit by concurrent TRM clinical use. In vitro and in vivo clinical evaluation of TRM in acute and chronic kidney disease however, is needed to strengthen the hypothesis of mitochondrial activity normalization as beneficial activity to complement, and hence proper nephron function.  Medical science owns the discovery of taurine transporter molecule from a P53 related sequence via a cisplatin kidney toxicity model. It is aimed that further research will unravel the health benefits of TRM use in complement associated nephropathies.