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Augmentation of cellular adenosine triphosphate levels in PC12 cells by extracellular adenosine
Author(s) -
Fujimori Hiroyuki,
PanHou Hidemitsu
Publication year - 2003
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.10174
Subject(s) - adenosine , adenosine kinase , extracellular , hypoxanthine , adenosine triphosphate , guanosine , inosine , biochemistry , purinergic signalling , uridine triphosphate , kinase , adenosine receptor , adenosine monophosphate , chemistry , biology , adenosine deaminase , nucleotide , receptor , enzyme , agonist , gene
The effects of extracellular adenosine (Ado) on cellular levels of adenosine triphosphate (ATP) in PC12 cells were studied. Ado and inosine but not adenine nucleotides, guanosine, cytosine, uridine, thymidine, and various P1 receptor agonists of Ado, significantly enhanced cellular ATP levels in PC12 cells by about 2.5‐fold. The ATP‐enhancing effect of Ado was potentiated by dipyridamole, an inhibitor of Ado uptake, and was also observed when PC12 cells were incubated in glucose‐free medium. These results suggest that augmentation of cellular ATP levels in PC12 cells by extracellular Ado might be acceleration of ATP synthesis through the Ado salvage system utilizing hypoxanthine‐guanine phosphoribosyltransferase rather than Ado kinase, since 5′‐iodotubercidin, an Ado kinase inhibitor, had no effect on the enhancement induced by Ado. Drug Dev. Res. 59:8–13, 2003. © 2003 Wiley‐Liss, Inc.