Studies on the Antagonism by Chloramphenicol of Carbon Tetra- chloride-Induced Damage: Examination of Mitochondrial Protein Syn-

Studies on the Antagonism by Chloramphenicol of Carbon Tetrachloride-Induced Damage: Examination of Mitochondrial Protein Synthesis. BRABEC, M.J., BRADLEY,~., AND BERNSTEIN, I.A.(1976). Toxicol. Appl. Pharmacol. 38, 157-167. The damage induced in the mitochondria of rat liver during intoxication by carbon tetrachloride is prevented by the administration of chloramphenicol early in the intoxication. The possibility that the protective ability of chloramphenicol lies in the compound’s ability to inhibit mitochondrial protein synthesis was eliminated by the failure of other inhibitors of mitochondrial protein synthesis, namely Tevenel, a chloramphenicol analog, and oxytetracycline, to prevent mitochondrial damage. Conversely, the optical isomer of chloramphenicol, which is not an inhibitor of mitochondrial protein synthesis, and does not possess antibiotic activity, does prevent mitochondrial damage during intoxication by Ccl,+. SKF 525A also preserves mitochondrial integrity, albeit not as well as chloramphenicol. Chloramphenicol, early in the course of intoxication, partially prevents the characteristic loss of protein synthesis after CC14. It was concluded that the protective action of chloramphenicol could be due to either an interdiction of a destructive event triggered by CC14, or to the preservation of the cellular repair processes being served by protein synthesis in the cytosol.