In a study appearing in the April 2007 issue of The FASEB Journal, scientists from Harvard University and the University of Pittsburgh have shown for the first time that the anti-inflammatory effects of carbon monoxide originate within cells’ own molecular engines, mitochondria. Specifically, mitochondria react to low levels of carbon monoxide by releasing chemical signals that reduce or shut down the body’s inflammatory response, raising the possibility for the development of new anti-inflammatory therapies, one of which may be low levels of inhaled carbon monoxide.>>> Discuss This Story