• Bulletin of the Korean Chemical Society
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• v.24 no.3
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• pp.350-356
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• 2003

The mechanism of the decomposition of a bronchodilator, S-nitroso-N-acetyl-D,L-penicillamine (SNAP) by a bronchoconstrictor, aqueous sulfite, has been investigated in detail. The decomposition was studied using a conventional spectrophotometer at 336 nm over the ranges: 0.010 ≤ $[S^{IV}]_T$ ≤ 0.045 mol $dm^{-3}$, 3.96 ≤ pH ≤ 6.80 and 15.0 ≤ θ≤ 30.0 ℃, 0.60 ≤ I ≤ 1.00 mol $dm^{-3}$, and at ionic strength 1.00 mol $dm^{-3}$ (NaCl). The rate of reaction is dependent on the total sulfite concentration and pH in a complex manner, i.e., $k_{obs}\;=\;k_1K_2[S^{IV}]_T/ ([H^+]\;+\;K_2)$. At 25.0 ℃, the second order rate constant, $k_1$, was determined as $12.5\;{\pm}\;0.15\;mol^{-1}\;dm^3\;s^{-1}$. ${\Delta}H^{neq}\;=\;+32\;{\pm}\;3 kJ\;mol^{-1}\;and\;{\Delta}S^{\neq}\;=\;-138\;{\pm}\;13\;J\;mol^{-1}K^{-1}$. The N-nitrosohydroxylamine-N-sulfonate ion was detected as an intermediate before the formation of any of the by-products, namely, N-acetyl-D,L-penicillamine. The effect of concentration of aqueous copper(Ⅱ) ions on this reaction was also examined at pH 4.75, but there was no dependence on $[Cu^{2+}]$. In addition, the $pK_a$ of SNAP was determined as 3.51 ± 0.06 at 25.4 ℃ [I = 1.0 mol $dm^{-3}$ (NaCl)].

• BMB Reports
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• v.39 no.1
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• pp.91-96
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• 2006

Previously, we have shown that nitric oxide (NO) directly activates the Maxi-K channels. In the present study, we have investigated whether NO has prolonged effects on the Maxi-K channels reconstituted in lipid bilayer. Application of S-nitroso-N-acetyl-D, L-penicillamine (SNAP), a NO donor, induced an immediate increase of open probability (Po) of Maxi-K channel in a dose-dependent manner. When SNAP was removed from the cytosolic solution, the Po did not simply returned to, but irreversibly decreased to a level lower than that of the control Po. At 0.2 mM, (Z)-[N-(3-Ammoniopropyl)-N-(n-propyl)amino] diazen-1-ium-1,2-diolate (PAPA-NO), another NO donor, produced a similar increase of Po and decrease of Po upon washout. The increasing effects of SNAP on Po were not blocked by either 50 U/ml superoxide dismutase (SOD) or 2 mM N-ethylmaleimide (NEM) pre-treatments. However, NEM appears to be ineffective when applied after SNAP. These results suggest that NO can modulate Maxi-K channel via direct interaction and chemical modification, such as S-nitrosylation in the brain.