Poly-S-Nitrosated Albumin as a Safe and Effective Multifunctional Antitumor Agent: Characterization, Biochemistry and Possible Future Therapeutic Applications

Figure 1

Differences in the mechanisms and consequences of NO traffic from Mono-SNO-HSA and Poly-SNO-HSA to cells. NO transfer from the SNO group of Cys-34 on Mono-SNO-HSA to the cell is partly mediated by the L-amino acid transporter (L-AT) via S-transnitrosation to free low molecular weight thiol. By contrast, NO transfer from Poly-SNO-HSA is mainly mediated by cell-surface protein disulfide isomerase (PDI) without S-transnitrosation to free low molecular weight thiol. The relatively slow transfer of NO from Mono-SNO-HSA avoids the presence of high intracellular NO concentrations and leads to cytoprotective activity through heme oxygenase-1 (HO-1) induction. On the other hand, the NO influx from Poly-SNO-HSA is very fast and pronounced and leads to cell death caused by apoptosis [14].