Key result
Thermodynamic and kinetic calculations demonstrate that N2O3 is not involved in in vivo nitrosation mechanisms and hemoglobin cannot catalyze its formation.
Key points are not available for this paper at this time.
Answers are grounded in this paper and cite their sources.
May challenge N2O3-based nitrosation models; leaves open validation of alternative in vivo pathways.
Nitrosothiols are powerful vasodilators. Although the mechanism of their formation near neutral pH is an area of intense research, neither the energetics nor the kinetics of this reaction or of subsequent reactions have been addressed. The following considerations may help to guide experiments. (1) The standard Gibbs energy for the homolysis reaction RSNO → RS(•) + NO(•)(aq) is +110 ± 5 kJ mol(-1). (2) The electrode potential of the RSNO, H(+)/RSH, NO(•)(aq) couple is -0.20 ± 0.06 V at pH 7. (3) Thiol nitrosation by NO(2)(-) is favorable by 37 ± 5 kJ mol(-1) at pH 7. (4) N(2)O(3) is not involved in in vivo nitrosation mechanisms for thermodynamic--its formation from NO(2)(-) costs 59 kJ mol(-1)--or kinetic--the reaction being second-order in NO(2)(-)--reasons. (5) Hemoglobin (Hb) cannot catalyze formation of N(2)O(3), be it via the intermediacy of the reaction of Hb[FeNO(2)](2+) with NO(•) (+81 kJ mol(-1)) or reaction of Hb[FeNO](3+) with NO(2)(-) (+88 kJ mol(-1)). (6) Energetically and kinetically viable are nitrosations that involve HNO(2) or NO(•) in the presence of an electron acceptor with an electrode potential higher than -0.20 V. These considerations are derived from existing thermochemical and kinetics data.
No takes yet. Share an insight, caveat, or question.
Willem H. Koppenol (2012) studied this question. Thermodynamic and kinetic calculations demonstrate that N2O3 is not involved in in vivo nitrosation mechanisms and hemoglobin cannot catalyze its formation.
Synapse has enriched 10 related papers. Consider them for comparative context: