Chloramphenicol induced inhibition of platelet protein synthesis: in vitro and in vivo studies.
Chloramphenicol (CAP), an antibiotic which causes various blood dyscrasias, was shown to inhibit in vitro protein synthesis of human blood platelets. The effect is dose- and time-dependent, it is reversible after incubation for 2 h, and is comparable with the suppression achieved by cycloheximide (CXM). Electron microscopic examination revealed swelling and destruction of mitochondria. Administration of CAP to dogs produced a progressive inhibition of platelet protein synthesis as shown by a reduction in the rate of [3H]leucine incorporation into protein. The maximal inhibitory effect of the antibiotic was reached 0.5-4.0 h after its administration, when minimal leucine incorporation values of 9-40% of the control were measured. The suppressive effect of CAP was followed by an overshoot in the incorporation of [3H]leucine, up to a maximum of 602% of the value at zero time of the experiment.
D000818:Animals; D001792:Blood Platelets / Q000032:analysis / Q000187:drug effects* / Q000648:ultrastructure; D002701:Chloramphenicol / Q000494:pharmacology*; D004285:Dogs; D006801:Humans; D007930:Leucine / Q000378:metabolism; D014176:Protein Biosynthesis; D014316:Tritium
D014316:Tritium; D002701:Chloramphenicol; D007930:Leucine