“…On the other hand, cysteamine has a protective feature against malaria infection, although the precise mechanisms remain to be elucidated (hatched arrows pointing upward). Unable to metabolize pantetheine in liver and kidney, very low tissue cysteamine levels (11) Increase in the level of reduced form of glutathione in tissues (12,17) g-glutamylcysteine synthetase activity (12) Delayed death caused by administration of lethal dose of paraquat (12) g-irradiation (12) 2,4,6-trinitrobenezene sulfonic acid (18) Schistosoma mansoni infection (17) Suppression of intestinal inflammation caused by administration of indomethacin and Schistosoma mansoni infection (17) unusual bone marrow stromal cells and chondrogenic transdifferentiation and calcification of aortic smooth muscle cells derived from ank/ank mice (20) incidence of colitis-associated colon cancer (24) granuloma formation in liver and spleen after the infection with Coxiella burnetii (21) the incidence of diabetes in NOD mice (23) Decrease in selenium-independent glutathione peroxidase activity and the GSTA3 protein level (22) Failure to induce inflammatory mediators including cytokines in response to stress (12,17,18,21,23,24) Induction of peroxisome proliferator activator receptor-g (18) activity and the GSTA3 protein (22). In humans, GSH/ GSSG levels are inversely correlated to VNN1 gene expression levels in chronic idiopathic thrombocytopenic purpura patients.…”