5-Iodotubercidin increases fatty acid oxidation activity and glycogen synthesis in hepatocytes. 5-Iodotubercidin is also a potent inhibitor of adenosine uptake into brain. Potent inhibitor of adenosine uptake into brain, and of adenosine kinase and subsequent metabolism of adenine nucleotides. In cultured rat hepatocytes, 5-iodotubercidin inhibits both acetyl-CoA carboxylase and de novo synthesis of fatty acids and cholesterol.1
Diadenosine polyphosphate functions as a second messenger in pancreatic cells, stimulates phospholipase D, changes intracellular calcium levels, induces nitric oxide release, activates 5′-nucleotidase, and inhibits adenosine kinase activity in vitro. Diadenosine polyphosphate is stored in secretory granules of thrombocytes, chromaffin, and neuronal cells. After release into the extracellular space, it affects a variety of biological activities in a wide range of target tissues. It appears to function as a second messenger in pancreatic cells. In rat liver cells. it stimulates phospholipase D and changes intracellular calcium levels. It has been shown to induce nitric oxide release from endothelial cells. In the nervous system it acts through various purinoceptors. It also activates 5′-nucleotidase and inhibits adenosine kinase activity in vitro. Ap4A is metabolized by soluble enzymes in the blood plasma and by membrane-bound ectoenzymes of a number of cell types including endothelial cells, smooth muscle cell.
