Abstract
THE metabolism of chloramphenicol has been studied extensively in animals and in human subjects, with the recognition of the glucuronide as the principal metabolic product1. In addition, a small amount of the amino diol hydrolysis product and free chloramphenicol were found in the urine1,2. However, little attention has been given to the metabolism of this compound where deficiencies exist in the conjugating mechanism. The normal adult cat has been reported to be deficient in its capacity to form glucuronides with a number of synthetic substrates3, and newborn animals generally have a low order of activity in the enzyme systems responsible for detoxication processes4. Consequently, the metabolism of chloramphenicol was investigated in the cat and in newborn human infants.
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