Toxicity of oxygen to mitochondrial respiratory activity in hypothermically perfused canine kidneys.
Respiratory activity of kidney cortex homogenates was measured after various periods of hypothermic pulsatile preservation of dog kidneys with cryoprecipitated plasma. There was a progressive loss of pyruvate plus malate-stimulated respiration (30 to 40% at 3 days and 70 to 80% at 5 days) and succinate-stimulated respiration (15 to 20% at 3 days and 50 to 60% at 5 days). Perfusion under conditions of low pO2 (30 to 40 mm Hg) or with inhibitors of the toxic effects of hyperbaric oxygen (CO2+ Mn2+) preserved homogenate respiratory activity better than with normal pO2 (150 mm Hg) or high pO2 (300 mm Hg). The results suggest that oxygen toxicity (lipid peroxidation) and the progressive loss of respiration in homogenates may be limiting factors in obtaining long-term preservation.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D003035:Cobalt / Q000494:pharmacology; D004140:Dinitrophenols / Q000494:pharmacology; D004285:Dogs; D007035:Hypothermia; D007668:Kidney / Q000378:metabolism*; D007672:Kidney Cortex / Q000166:cytology; D008345:Manganese / Q000494:pharmacology; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D009840:Oligomycins / Q000494:pharmacology; D010100:Oxygen / Q000633:toxicity*; D010101:Oxygen Consumption / Q000187:drug effects; D014021:Tissue Preservation
D004140:Dinitrophenols; D009840:Oligomycins; D003035:Cobalt; D008345:Manganese; D000244:Adenosine Diphosphate; D010100:Oxygen