In vitro Action of Chloramphenicol and Chloramphenicol-Analogues on the Metabolism of Human Immature Red Blood Cells

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Abstract
Chloramphenicol suppresses uptake and intracellular utilization of Fe59 by human bone marrow cells and reticulocytes in vitro when used in high concentrations for short periods of time. It is possible that a similar suppression may occur in vivo with low concentrations at prolonged periods of time. The metabolic products of chloramphenicol, with the exception of nitro-phenylamine (a derivative found only in trace amounts in vivo), are inert in the test systems used here. Chloramphenicol-induced inhibition of Fe uptake appears to be caused by a surface defect while inhibition of Fe utilization is related to protein synthesis. The development of cellular vacuolization, erythroid suppression and aplastic anemia do not appear to be caused by change in Fe metabolism, since some other drugs not known to be associated with the development of aplastic anemia were found also to suppress Fe metabolism in vitro.