Carbon monoxide, toxic by-product or protective gaseous monoxide?

摘要

The toxic properties of carbon monoxide (CO) are well characterized. The binding of CO to hemoglobin interferes in a concentration-dependent manner with oxygen transport and oxygen delivery; furthermore, inhibition of the cyto-chrome c oxidase contributes to cell hyp-oxia. At high concentrations, CO acts as a potent asphyxiant associated with a number of clinical symptoms, including dizziness, loss of consciousness, and death, following prolonged or excessive exposure. Symptoms of CO poisoning in humans usually begin to appear with car-boxyhemoglobin (CO-Hb) levels of 20%. But even low CO-Hb levels (2% to 6%) are known to reduce exercise capacity (1) and induce ST changes in patients with coronary artery disease (2).Endogenous production of CO arises primarily (>85%) from the degradation of hemoglobin and other heme proteins by heme oxygenase (HO) enzymes.