Metabolism
Hydrogen sulfide stimulates lipid biogenesis from glutamine that is dependent on the mitochondrial NAD(P)H pool
Mammalian cells synthesize H2S from sulfur-containing amino acids and are also exposed to exogenous sources of this signaling molecule, notably from gut microbes. As an inhibitor of complex IV in the electron transport chain, H2S can have a profound impact on metabolism, suggesting the hypothesis that metabolic reprogramming is a primary mechanism by which H2S signals. In this study, we report that H2S increases lipogenesis in many cell types, using carbon derived from glutamine rather than from glucose.Hydrogen sulfide perturbs mitochondrial bioenergetics and triggers metabolic reprogramming in colon cells
Unlike most other tissues, the colon epithelium is exposed to high levels of H2S derived from gut microbial metabolism. H2S is a signaling molecule that modulates various physiological effects. It is also a respiratory toxin that inhibits complex IV in the electron transfer chain (ETC). Colon epithelial cells are adapted to high environmental H2S exposure as they harbor an efficient mitochondrial H2S oxidation pathway, which is dedicated to its disposal. Herein, we report that the sulfide oxidation pathway enzymes are apically localized in human colonic crypts at the host–microbiome interface, but that the normal apical-to-crypt gradient is lost in colorectal cancer epithelium.Introduction to the Thematic Minireview Series: Redox metabolism and signaling
In this sequel to the thematic collection of Minireviews on redox metabolism and signaling published last year, five articles plumb the redox metabolic pathways relevant to cell proliferation, stress response, and survival post-detachment from the extracellular matrix. The sixth article provides unexpected insights into the hepatic NAD(P)ome, revealing that more than half of these proteins reside outside the cytoplasmic and mitochondrial compartments, pointing to the paucity of knowledge on their functions.
