Carbon monoxide and energy metabolism

Adenosine triphosphate (ATP) quantification is an indirect way to assess cellular energy metabolism status and a first step to disclose energy metabolic response. Oxidation of carbon fuel generates ATP directly (glycolysis followed by anaerobic generation of lactate) or by promoting ion gradients (mitochondrial aerobic processes via tricarboxylic acid cycle and oxidative phosphorylation [OXPHOS]). In primary culture of mouse astrocytes, carbon monoxide (CO) also increased cellular levels of ATP under basal conditions. CO appears to reinforce metabolism toward OXPHOS rather than glycolysis with anaerobic lactate formation. This CO effect is accompanied by an increase in mitochondrial population and prevention against oxidative stress-induced apoptosis in astrocytes. CO might directly or indirectly modulate pentose phosphate pathway, in order to maintain cellular redox balance, via reinforcing glutathione recycling. The role of CO in peroxisome is a biological subject yet to be explored and can be associated with CO control of lipid metabolism.