Figure 9. Scheme of PABA/NO effects on Ca²⁺/NO homeostasis in HL60 cells.

PABA/NO effects start as extracellular NO-mediated (from spontaneous decomposition) surface protein-thiol modifications. Intracellular PABA/NO spontaneously (or under GSTP-catalysis) generates NO and stable nitro-aromatic compound(s) (PABA-SG). This can inhibit SERCA initiating a release of Ca²⁺ from the sarcoplasmic (endoplasmic) reticulum. The latter activates CaM and, consequently eNOS producing an NO burst. Increases of NO above threshold levels result in eNOS inhibition through its S-nitrosylation/glutathionylation. Once NO levels start to decline, spontaneous or catalyzed deglutathionylation of eNOS results in its reactivation to maintain steady state NO levels.