Influence of cytarabine on mitochondrial function and mitochondrial biogenesis.
Although replication of nuclear DNA is inhibited by cytarabine (ara-C), protein synthesis in the nucleocytoplasm appears to continue unabated for the duration of at least the time of the normal cell cycle. ara-C treatment of human leukemic cells resulted in increased mitochondrial membrane potential and adenosine-5'-triphosphate (ATP) production and increased activity of enzymes, coded on nuclear DNA (citrate synthetase), as well as of enzymes with subunits coded on mitochondrial DNA (cytochrome c oxidase). These mitochondrial changes occurred during a period of cell-cycle arrest, while cell size and cellular protein content continued to increase. These phenomena appeared to precede the ultimate cell death.
D002460:Cell Line; D002950:Citrate (si)-Synthase / Q000378:metabolism; D003561:Cytarabine / Q000494:pharmacology*; D003576:Electron Transport Complex IV / Q000378:metabolism; D006801:Humans; D007425:Intracellular Membranes / Q000187:drug effects; D007938:Leukemia / Q000188:drug therapy / Q000473:pathology; D008564:Membrane Potentials / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects*; D011506:Proteins / Q000378:metabolism
D011506:Proteins; D003561:Cytarabine; D003576:Electron Transport Complex IV; D002950:Citrate (si)-Synthase