Abstract
Guinea pig kidney cortical slices accumulate α-ketoglutarate from the medium against a concentration gradient, whereas citrate is not accumulated against a gradient. The concentration of citrate in kidney slices is increased by 0·05–3·6 mM phenolsulfonphthalein. PSP also stimulates the accumulation of α-KG by kidney cortical slices, simultaneously inhibiting α-KG utilization and respiration. At 0° PSP does not affect the tissue concentration and utilization of citrate and α-KG. One to nine mM probenecid greatly decreases the concentration of citrate in kidney slices; 1–3 mM probenecid has no effect on the utilization of citrate, but 9 mM probenecid inhibits utilization by 25 per cent and respiration by 40 per cent. Probenecid inhibits the accumulation of α-KG in kidney slices, simultaneously inhibiting α-KG utilization and respiration. At 0° probenecid has only a slight decreasing effect on citrate concentration of the slices. PSP inhibits the oxidation of α-KG and succinate by kidney mitochondria, whereas citrate oxidation is more resistant. Probenecid inhibits the oxidation of α-KG by kidney mitochondria, whereas citrate and succinate oxidations are more resistant to probenecid. The results demonstrate that PSP and probenecid act both intracellularly at mitochondrial sites and at outer cell membrane.
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