This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on Web of Science (73)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

A Consequence of Mitochondrial Injury

Adel A. Yunis, MD; Una S. Smith, PhD; Alberto Restrepo, MD

Arch Intern Med. 1970;126(2):272-275.

Abstract
Chloramphenicol is a potent inhibitor of mitochondrial protein synthesis. Recent studies on rabbit and human bone marrow mitochondria strongly suggest a relationship between inhibition of protein synthesis and myelotoxicity from chloramphenicol. A thorough electron microscopic study of bone marrow mitochondria derived from patients receiving chloramphenicol indicates that this drug induces ultrastructural modifications resulting in an increase in the density of the mitochondrial matrix. Excellent correlation is observed between the extent of the ultrastructural changes and serum levels of free chloramphenicol. The results lend further support to the hypothesis that reversible bone marrow suppression from chloramphenicol results from inhibition by the drug of mitochondrial protein synthesis.

Author Affiliations
Miami, Fla; Medellin, Colombia

From the Department of Medicine and Biochemistry and Howard Hughes Medical Institute, University of Miami School of Medicine, Miami, Fla (Drs. Yunis and Smith); and the Department of Medicine, University of Antioquia, Medellin, Colombia (Dr. Restrepo).

Footnotes
Received for publication Feb 9, 1970; accepted April 3.

Reprint requests to University of Miami, PO Box 875, Biscayne Annex, Miami, Fla 33152 (Dr. Yunis).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Erythroid dysplasia, megaloblastic anemia, and impaired lymphopoiesis arising from mitochondrial dysfunction
Chen et al.
Blood 2009;114:4045-4053.
ABSTRACT | FULL TEXT  

Ex vivo zidovudine (AZT) treatment of CD34+ bone marrow progenitors causes decreased steady state mitochondrial DNA (mtDNA) and increased lactate production
Lewis et al.
Hum Exp Toxicol 2004;23:173-185.
ABSTRACT  

Stratified Outcome Comparison of Clindamycin-Gentamicin vs Chloramphenicol-Gentamicin for Treatment of Intra-abdominal Sepsis
Lennard et al.
Arch Surg 1985;120:889-898.
ABSTRACT  

Vacuolization of Leukocytes and Bone Marrow Aplasia Due to Chloramphenicol Toxicity
Awwaad et al.
CLIN PEDIATR 1975;14:499-506.
 

Parenteral Clindamycin Therapy for Severe Anaerobic Infections
Chow et al.
Arch Intern Med 1974;134:78-82.
ABSTRACT  

Chloramphenicol-lnduced Bone Marrow Suppression
JAMA 1970;213:1183-1184.
ABSTRACT