Prominent glutamine oxidation activity in mitochondria of avian transplantable hepatoma induced by MC-29 virus

Abstract

Well coupled mitochondria were isolated from transplantable chicken hepatoma induced by MC‐29 virus. The mitochondrial phosphate‐dependent and phosphate‐independent glutaminase activities were increased compared with those from normal chicken liver. Glutamate dehydrogenase was undetectable in the tumor mitochondria. Oxypolarographic tests showed the following: (1) glutamine oxidation was prominent in the tumor mitochondria and was mediated through an NAD‐linked reaction, while mitochondria from the liver showed a feeble glutamine oxidation; (2) glutamine oxidation by tumor mitochondria was inhibited either by aminooxyacetate, inhibitor of transaminases, or prior incubation of mitochondria with DON (6‐diazo‐5‐oxonorleucine), which inhibited mitochondrial glutaminases. Bromofuroate, inhibitor of glutamate dehydrogenase, had little or no effect; and (3) glutamate oxidation was also inhibited by aminooxyacetate, while it was not affected by DON. These findings clearly show a high glutamate oxidation activity in the hepatoma and indicate that the product of glutamine hydrolysis, glutamate, is catabolized via transamination in the mitochondria to supply ATP.