Oxyhemoglobin, reaction with nitric oxide

In blood-containing vascular beds, the inactivation of nitric oxide by oxygen is of minor importance because of the rapid and irreversible reactions of nitric oxide with oxyhemoglobin in red blood cells. Any nitric oxide that diffuses into the vascular lumen will be quickly destroyed, making blood vessels effective sinks for nitric oxide. The half-life of nitric oxide is sufficiently long that nitric oxide diffusing into the vascular smooth muscle could also diffuse back out to the lumin to be inactivated by hemoglobin in red blood cells. 

The second reaction and certainly the major route for the destruction of nitric oxide in vivo is the fast and irreversible reaction with oxyhemoglobin (Hb) or oxymyoglobin to produce nitrate. 

Fig. 3. Production of reactive species. (A) ROS can be produced from the weak radical oxygen in the mitochondria and endoplasmic reticulum, by various enzymatic reactions, and from oxyhemoglobin. Normally, nontoxic hydrogen peroxide can give rise to the powerful hydroxyl radical in the presence of transition metals (R5). Oxygen can also be induced to react with biomolecules by transition metals and enzymes. RNS can be produced by reaction of superoxide anion radical with the weak radical nitric oxide. These can react to form the powerful oxidant peroxynitrite/peroxynitrous acid, which can cause formation of other radicals, some with longer lives. See the text for details. SOD, superoxide dismutase. (B) Myeloperoxidase in leukocytes can produce the reactive species hypochlorous acid and tyrosyl radical. Unpaired electrons are indicated by the dense dots and paired electrons by the light ones.

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