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© 1984 Oxford University Press

research-article

Recovery from Amiodarone-Induced Lipidosis in Laboratory Animals: A Toxicological Study

G. MAZUE, P. VIC, D. GOUY, B. REMANDET, F. LACHERETZ, J. BERTHE, G. BARCHEWTTZ and J. P. GAGNOL

Centre de Recherches, CLIN-MIDY Groupe Sanofi, Montpellier, France

Recovery from Amiodarone-lnduced Lipkiosis in Laboratory Animals: A Toxicological Study. MAZUE, G., VIC, P, GOUY, D., REMANDET, B., LACHERETZ, F., BERTHE, J., BARCHEWTTZ, G., AND GAGNOL, J. P. (1984). Fundam. Appl. Toxicol. 4, 992–999. Numerous amphiphilic cationic drugs cause lipid–lysosomal storage in animal tissues; one of these drugs is amiodarone, a major antiarrhythmic agent. The toxicological effects of amiodarone were studied in three animal species (rats, dogs, and monkeys). It was shown that sublethal dose levels of amiodarone induced lipid storage in a great variety of tissues in rats (Fischer and Sprague-Dawley strains) and dogs. However, this change was not observed in baboons and Wistar rats. This storage, essentially characterized by lamellated inclusions, affected foamy macrophages, and at a later phase multiple cell types. Tissue biochemical analysis provided evidence of the phospholipidic nature of the storage. In addition, amiodarone induced an increased cholesterolemia and marked modifications of the lipoproteinogram. The kinetics of lipid storage was demonstrated following oral administration of amiodarone. After jejunal absorption, lipid storage occurred in the mesenteric lymph nodes followed by widespread deposition in the other lymph nodes and tissues, particularly in the lung. A complete recovery from lipid storage was observed in dogs and rats. Finally, an investigation of a correlation between animal and man by means of long-terra experiments is proposed.


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