Isolation of chloramphenicol-resistant variants from a human cell line.
Variant clones resistant to 40 microng/ml chloramphenicol were isolated from the human cell line VA2-B after treatment with either ethyl methanesulfonate or N-methyl-N'-nitro-N-nitrosoguanidine. Among 17 clones analyzed, one variant, CAP-23, was investigated in detail. CAP-23 cells in the presence of 40 or 100 microng/ml chloramphenicol grew at essentially the same rate as cells in the absence of the drug; chloramphenicol resistance persisted even after 20 generations in the absence of the drug. No obvious morphological changes in mitochondria were observed by electron microscopy of thin sections of CAP-23 cells. In vivo mitochondrial protein synthesis in CAP-23 cells was inhibited little, if any, by chloramphenicol, and the variant showed and partial cross resistance to mikamycin and carbomycin. In vitro protein synthesis in mitochondria isolated from CAP-23 cells showed, likewise, low levels of inhibition by chloramphenicol. This suggests that the drug resistance of the variant CAP-23 is due to altered mitochondria.
D002460:Cell Line; D002701:Chloramphenicol / Q000494:pharmacology*; D004272:DNA, Mitochondrial; D004351:Drug Resistance; D005020:Ethyl Methanesulfonate / Q000494:pharmacology; D014644:Genetic Variation; D007933:Leucomycins / Q000494:pharmacology; D008769:Methylnitronitrosoguanidine / Q000494:pharmacology; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D009154:Mutation; D014176:Protein Biosynthesis; D014769:Virginiamycin / Q000494:pharmacology
D004272:DNA, Mitochondrial; D007933:Leucomycins; D014769:Virginiamycin; D008769:Methylnitronitrosoguanidine; D002701:Chloramphenicol; D005020:Ethyl Methanesulfonate