Abstract
Ferrochelatase activity was determined in bone marrow mitochondria of dogs receiving 100 mg. of chloramphenicol per kilogram per day and of control animals. Those animals receiving chloramphenicol for 3 weeks exhibited a 65 to 90 per cent decrease in ferrochelatase activity as compared to the controls; this enzymic activity returned to normal levels 8 weeks after discontinuation of treatment. Accompanying the drop in ferrochelatase activity was a marked elevation of the level of free erythrocyte protoporphyrin and an increase in stainable bone marrow iron, findings consistent with a block in the final step of heme synthesis. Two of the 3 dogs receiving chloramphenicol showed a significant retiwlocytopenia; the reticulocyte count returned to normal 2 weeks after cessation of chloramphenicol therapy. No significant alteration in the white cell and platelet values were observed. Whatever the mechanism involved, it is hypothesized that the suppression of ferrochelatase activity by chloramphenicol accompanied by a block in the last step of heme synthesis offers a reasonable explanation for the apparent vulnerability of the erythroid cells to the drug.
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