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Erythromycins selective toxicity

Macrolides, both erythromycin and others, inhibit the synthesis of bacterial proteins. The primary mechanisms of protein synthesis are identical in humans and bacteria. However, there is a significant difference that allows a specific antibiotic to exhibit selective toxicity with respect to bacteria. [Pg.467]

Macrolides bind to the SOS ribosomal subunit of bacteria but not to the SOS mammalian ribosome this accounts for its selective toxicity. Binding to the ribosome occurs at a site near peptidyltransferase, with a resultant inhibition of translocation, peptide bond formation, and release of oligopeptidyl tRNA. However, unlike chloramphenicol, the macrolides do not inhibit protein synthesis by intact mitochondria, and this suggests that the mitochondrial membrane is not permeable to erythromycin. [Pg.548]

CLARITHROMYCIN, ERYTHROMYCIN VINCA ALKALOIDS -VINBLASTINE, VINCRISTINE, VINORELBINE t adverse effects of vinblastine and vincristine Inhibition of CYP3A4-mediated metabolism. Also inhibition of P-gp efflux of vinblastine Monitor FBCs. Watch for early features of toxicity (pain, numbness, tingling in the fingers and toes, jaw pain, abdominal pain, constipation, ileus). Consider selecting an alternative drug... [Pg.517]


See other pages where Erythromycins selective toxicity is mentioned: [Pg.514]    [Pg.92]    [Pg.489]    [Pg.67]    [Pg.107]    [Pg.67]    [Pg.149]    [Pg.342]    [Pg.1419]    [Pg.159]    [Pg.197]    [Pg.303]    [Pg.385]    [Pg.168]    [Pg.456]   
See also in sourсe #XX -- [ Pg.5 , Pg.261 , Pg.262 ]




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