Acetyl Coenzyme A (trisodium)

Acetyl-coenzyme A (Acetyl-CoA) trisodium is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A trisodium, regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A trisodium is also a key precursor of lipid synthesis^[1][2][3][4]. In Vitro: Acetyl coenzyme A trisodium increases cytoplasmic protein acetylation in starved U2OS cells while reducing starvation-induced autophagic fluxes. (U2OS cells stably expressing GFP-LC3 and are microinjected with Acetyl coenzyme A trisodium; incubated in nutrient-free conditions in the presence of 100 nM BafA1 and fixed after 3 h)^[2]. In Vivo: Acetyl coenzyme A trisodium blunts pressure overload-induced cardiomyopathy in a mice cardiac pressure overload model by Suppressing maladaptive autophagy^[2][3]. Mice deprived of food (but with access to water ad libitum) for 24 h exhibit a significant reduction in total Acetyl coenzyme A trisodium levels in several organs, including the heart and muscles, corresponding to a decrease in protein acetylation levels. However, the same experimental conditions have no major effects on Acetyl coenzyme A trisodium concentrations in the brain and actually increase hepatic Acetyl coenzyme A trisodium and protein acetylation levels^[4].