Chloramphenicol Induced Inhibition of Platelet Protein Synthesis: in Vitro and in Vivo Studies

Authors

  • Galila Agam,

    1. Department of Medicine ‘B’, Hematology Clinic, Hasharon Hospital, Beilinson Medical Center, Petah-Tiqva, and Tel-Aviv University Medical School, Israel
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  • S. Gasner,

    1. Department of Medicine ‘B’, Hematology Clinic, Hasharon Hospital, Beilinson Medical Center, Petah-Tiqva, and Tel-Aviv University Medical School, Israel
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  • Hana Bessler,

    1. Department of Medicine ‘B’, Hematology Clinic, Hasharon Hospital, Beilinson Medical Center, Petah-Tiqva, and Tel-Aviv University Medical School, Israel
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  • Pnina Fishman,

    1. Department of Medicine ‘B’, Hematology Clinic, Hasharon Hospital, Beilinson Medical Center, Petah-Tiqva, and Tel-Aviv University Medical School, Israel
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  • M. Djaldetti

    Corresponding author
    1. Department of Medicine ‘B’, Hematology Clinic, Hasharon Hospital, Beilinson Medical Center, Petah-Tiqva, and Tel-Aviv University Medical School, Israel
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Professor M. Djaldetti, Department of Medicine ‘B’, Hasharon Hospital, Petah-Tiqva, Israel.

Summary.

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.

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