The adenine nucleotide catabolism in nonphosphorylating mitochondria of different tissues.
The degradation of endogenous adenine nucleotides was compared in mitochondria isolated from mouse and rat liver, rat renal cortex and solid hepatoma. Mitochondria were incubated for 30 min at 37 degrees C in the presence of carboxyatractyloside and oligomycin. In rat liver mitochondria ATP, ADP and AMP were degraded by about 25% each, whereas in kidney and hepatoma mitochondria a rapid decline of ATP and ADP but no change in the AMP contents were observed. Main products formed were adenosine, inosine and hypoxanthine in all mitochondria examined. Compartment studies revealed that the main route of intramitochondrial adenine nucleotide catabolism seems to proceed via AMP dephosphorylation and subsequent adenosine deamination.
Ziegler
M
M
Institut für Biochemie, Bereich Medizin Charité, Humboldt Universität, Berlin, DDR.
Dubiel
W
W
Henke
W
W
Jung
K
K
Pimenov
A M
AM
Tikhonov YuV
Togusov
R T
RT
Gerber
G
G
D000227:Adenine Nucleotides / Q000378:metabolism*; D000818:Animals; D001278:Atractyloside / Q000031:analogs & derivatives / Q000494:pharmacology; D007672:Kidney Cortex / Q000378:metabolism*; D007700:Kinetics; D008114:Liver Neoplasms, Experimental / Q000378:metabolism*; D051379:Mice; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000378:metabolism*; D009840:Oligomycins / Q000494:pharmacology; D009928:Organ Specificity; D051381:Rats
D000227:Adenine Nucleotides; D009840:Oligomycins; D001278:Atractyloside; C003853:carboxyatractyloside