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Low-molecular-weight S-nitrosothiols and blood vessel injury
Philip A. Marsden
Philip A. Marsden
Published September 4, 2007
Citation Information: J Clin Invest. 2007;117(9):2377-2380. https://doi.org/10.1172/JCI33136.
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Commentary

Low-molecular-weight S-nitrosothiols and blood vessel injury

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Abstract

S-nitrosothiol signaling reactions are argued to play key modulatory roles in mediating the actions of NOS in health and disease. A report by Palmer et al. in this issue of the JCI provides new insight into the in vivo biology of S-nitrosothiols (see the related article beginning on page 2592). The authors examine the chronic effects of exogenous nitrosothiol therapy and demonstrate that the commonly used antioxidant N-acetylcysteine (NAC) induces pulmonary arterial hypertension in mice. Importantly, the authors argue that the vascular pathology they observe in the lungs of these animals is functionally and morphologically equivalent to that observed in chronic hypoxia. These findings raise the concern that chronic NAC therapy may induce similar vascular pathology in patients.

Authors

Philip A. Marsden

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Figure 1

S-nitrosothiols and the Hb O2 cycle.

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S-nitrosothiols and the Hb O2 cycle.
               
The synthesis of S...
The synthesis of SNO-Hb is favored in the highly oxygenated R structure of tetrameric Hb. SNO-Cysβ93 is buried deep within oxygenated Hb. SNO-Hb transports NO to the microcirculation. Less than 1% of Hb carries NO. With a switch in Hb to the deoxygenated T structure when O2 concentrations fall, the S-nitrosothiol group is exposed and transferred to other thiol acceptors. NAC can serve as a pharmacological bait and forms SNOAC.

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