Abstract
A possible explanation for the previously reported “synergistic toxicity” of normally non-lethal doses of anti-inflammatory drugs in rats with arthritis induced by 6-sulfonanilamidoindazole (SAI) was sought by examining the drug-metabolizing capability of these arthritic rats. Rats given SAI had prolonged (10-fold) sleeping times when challenged with pentobarbital. The apparent plasma half-life of phenylbutazone was increased from 4.2 to 17.4 hr in SAI-treated rats. The mean “steady state” plasma concentration of phenylbutazone was two to three times higher in SAI-treated rats. The N-demethylation of aminopyrine in vitro by liver 9000 g supernatant enzyme preparations proceeded at a rate of approximately 25 per cent that of control rats. The results suggest that SAI-treated rats are defective in their drug-metabolizing capability.
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