Role of adenine nucleotide translocase in metabolic change caused by ischemia.

Abstract

Inhibition of adenine nucleotide translocase by elevated levels of long chain acyl-CoA esters has been shown to occur during the onset of ischemia in experiments conducted on dogs. Other findings indicate that, as a consequence of translocase inhibition, the production of mitochondrial creatine phosphate was abolished and, in this manner, respiration was slowed to state 4 or an ischemic-like condition. A variety of biochemical, hemodynamic, and ultrastructural evidence further suggest that this inhibition of adenine nucleotide transport in and out of the heart mitochondria may be the initial and key disturbance which "triggers" the more drastic metabolic changes known to occur as the degree of ischemia becomes more severe. The mitochondrial "damage" caused by long chain acyl-CoA ester inhibition of adenine nucleotide translocase appears to be reversible by carnitine.

• Authors: A L Shug, J R Koke, J D Folts, N Bittar
• Journal: Recent advances in studies on cardiac structure and metabolism (Recent Adv Stud Cardiac Struct Metab) Vol. 10 Pg. 365-78 ( 1975) ISSN: 0363-5872 [Print] United States
• PMID: 1208988 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Oleic Acids
• Phosphocreatine
• Atractyloside
• Adenosine Diphosphate
• Mitochondrial ADP, ATP Translocases
• Nucleotidyltransferases
• Carnitine
• Coenzyme A

Topics

• Adenosine Diphosphate (metabolism)
• Animals
• Atractyloside (pharmacology)
• Carnitine (pharmacology)
• Cattle
• Coenzyme A (pharmacology)
• Coronary Disease (metabolism)
• Dogs
• Hemodynamics
• Mitochondria, Muscle (metabolism)
• Mitochondrial ADP, ATP Translocases (antagonists & inhibitors, metabolism)
• Nucleotidyltransferases (metabolism)
• Oleic Acids (pharmacology)
• Oxygen Consumption (drug effects)
• Phosphocreatine (biosynthesis)
• Time Factors