Acetyl-Coenzyme A Assay Kit has been used to quantify the level of acetyl-CoA in astrocytes exposed to recombinant HIV protein Tat and Cocaine. It has also been used to study the mitochondrial metabolism by evaluating the levels of acetyl-CoA using hypoxia induced stress in primary human ventricular cardiomyocytes.
Acetyl-CoA is an essential cofactor and carrier of acyl groups in enzymatic acetyl transfer reactions. It is formed either by the oxidative decarboxylation of pyruvate in mitochondria, by the oxidation of long-chain fatty acids, or by the oxidative degradation of certain amino acids. Acetyl-CoA is the starting compound for the citric acid cycle (Kreb′s cycle). It is also a key precursor in lipid biosynthesis, and the source of all fatty acid carbons. Acetyl-CoA positively regulates the activity of pyruvate carboxylase. It is a precursor of the neurotransmitter acetylcholine. Histone acetylases (HAT) use Acetyl-CoA as the donor for the acetyl group used in the post-translational acetylation reactions of histone and non-histone proteins.
Acetyl-Coenzyme A acts as an indicator of fat, sugar, and protein levels and shows up on the nutritional status. Thus, starvation greatly reduces the level of acetyl-CoA, which stimulates the process of autophagy. In lowered glucose condition, acetyl-CoA participates in the production of ATP. Increased acetyl-CoA levels are observed in prostate cancer due to elevated fatty acid utilization and thus provides an additional energy source for the tumor cell growth. Nutrition deprivation, changes the levels of certain metabolites, including acetyl-CoA, which stimulates epigenetic modifications that would affect the central nervous system.
