The effects of acidosis on canine hepatic and renal oxidative phosphorylation.
The intracellular effects of acidosis remain poorly defined. To examine the effects of acidosis on oxidative phosphorylation, liver biopsies and weight nephrectomies were performed on 10 adult German shepherd dogs. The mitochondria were isolated from each tissue and their respiratory activity was studied by the polarographic technique with the pH of the reaction media varied from 5.5 to 8.0. Glutamate and succinate substrates were employed. Results showed a dramatic reduction in the efficiency of oxygen utilization by mitochondria with glutamate as the reaction medium became more acidic. The efficiency of succinate oxidation was significantly (P less than 0.01) preserved. These findings were confirmed by both the respiratory control indices and by ADP:O ratios. Acidosis appears to result in severe inhibition of NAD-linked energy substrate oxidation.
D000138:Acidosis / Q000378:metabolism*; D000244:Adenosine Diphosphate / Q000378:metabolism; D000818:Animals; D004285:Dogs; D005971:Glutamates / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007668:Kidney / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D008930:Mitochondria, Liver / Q000378:metabolism; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption; D013386:Succinates / Q000378:metabolism
D005971:Glutamates; D013386:Succinates; D000244:Adenosine Diphosphate