Abstract
Cinoxacin (CINX) is known to be secreted by renal tubules and to cause renal damage at very high doses only in rats. In order to know the mode of CINX transport and its effect on cellular metabolism in the kidney, effects of CINX on p-aminohippurate (PAH) transport and cellular function were examined using renal cortical slices of rat and rabbit as compared with nalidixic acid (NA) with no nephrotoxic action. CINX competitively inhibited PAH accumulation in rat renal slices without affecting the Na gradient across cell membranes. Incubating the slices with CINX caused an accumulation of CINX which was inhibited by PAH. Effects of+CINX mM) on water content, inulin space, transports of Na+ and K, ATP content and oxygen consumption of the slices werç not detected in rat renal slices, but CINX suppressed the Na transport in rabbit kidney slices. On the other hand, NA (5 mM) depressed all parameters mentioned above in rat and water content and Na transport in rabbit. CINX and NA had no effect on the release of N-acetyl-β-D-glucosaminidase from renal slices of rat and rabbit. These results suggest that CINX is transported by the same process as PAH and has no effect on cellular function. So, the renal damage caused by CINX in rat appears to be due to physical trauma resulting from deposition of CINX crystals in the urinary tract.
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