Carbon monoxide (CO) can arrest cellular respiration, but paradoxically is also synthesized endogenously by heme oxygenase type 1 (Ho-1) in response to conditions of low oxygen. In the May Nature Medicine Tomoyuki Fujita and colleagues at Columbia University, New York suggest a therapeutic potential for CO, reporting that mice lacking the gene for Ho-1 exposed to ischemic stress can recover by inhaling CO.

Fujita et al tested a murine model of lung ischaemia/reperfusion injury and observed a 7–8-fold increase in the expression of HO-1 mRNA in wild type mice. Only 12% of these mice died as a result of the injury. In contrast HO-1-deficient mice subjected to an identical insult all died within 24 hours. Subsequent experiments in which HO-1-deficient mice received CO by inhalation (0.1% or 500–1000 ppm) reduced the mortality by 50%.

The study suggests that CO activates soluble guanylate cyclase thereby suppressing hypoxic induction of the...

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