Extra attention to signs of suicidality is especially called for in the clinical setting and in the L-755,507 monitoring of patients during initiation with SSRI therapy. However, the effect could be present with other treatments for depression, and therefore the specificity of this effect needs to be studied further. Thalassemia is a hematological genetic disorder caused by deficiency of alpha or beta chains of hemoglobins, which are known as alpha or beta thalassemia, respectively. Beta thalassemia/hemoglobin E is a form of beta thalassemia commonly found in South East Asia including Thailand. In this disease, the synthesis of beta globin chain is insufficient, causing aggregations of excessive unpaired alpha globin chains. The alpha chain aggregates could produce reactive oxygen species, leading to oxidative stress-induced red blood cell senescence characterized by externalization and release of phosphatidylserine. The oxidation-damaged erythrocytes are subject to premature phagocytic destruction in the spleen and, therefore, have a short life span in circulation. These pathological events underline severe anemia and splenomegaly observed in beta thalassemia/Hb E patients. Reduced glutathione is an important endogenous antioxidant in all cell types including erythrocytes. Levels of GSH inside the cells are tightly regulated by the rate of GSH synthesis and GSH efflux via membrane transporters, namely multidrug resistance-associated protein, cystic fibrosis transmembrane conductance regulator, and organic anion transporting polypeptide. Among MRPs, MRP 1, MRP 2, MRP4 and MRP 5 can transport GSH and other glutathione conjugates including oxidized glutathione. In addition to serving as chloride channels, CFTR plays an important role in exporting GSH and glutathione conjugates from airway epithelial cells into airway surface liquid, which provides protection of the airways from oxidative damage during infection and inflammation. Indeed, effluxes of GSH and GSSG precede oxidative stress-induced apoptosis of several cell types, including L-Aspartic acid astrocytes, endothelial cells, epithelial cells and erythrocytes. Pharmacological blockage and genetic ablation of glutathione efflux transporters have been shown to prevent oxidative stress-induced apoptosis in renal epithelial cells by preventing effluxes of GSH and GSSG, which, in turn, reduce production of reactive oxygen species. GlyH-101 and MK571 are well-characterized inhibitors of CFTR and MRP, respectively. GlyH-101 is a CFTR inhibitor discovered by high-throughput screening. Previous studies have shown that GlyH-101 blocks CFTR by occluding the external pore of CFTR and that GlyH-101 administration prevents cholera toxin-induced intestinal fluid secretion in mouse closed loop models.