Chapter 4 Carbon Monoxide and Energy Metabolism Book Editor(s):Binghe Wang, Binghe Wang Georgia State University, Atlanta, GA, USASearch for more papers by this authorLeo E. Otterbein, Leo E. Otterbein Beth Israel Deaconess Medical Center, Boston, MA, USASearch for more papers by this author First published: 07 May 2022 https://doi.org/10.1002/9781119783435.ch4 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Abstract 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. Carbon Monoxide in Drug Discovery: Basics, Pharmacology, and Therapeutic Potential RelatedInformation