The glycylcyclines are tetracycline analogs that retain activity against tetracycline-resistant organisms containing genes mediating drug efflux or ribosomal protection. The drug tigecycline (tiga-cyl) is FDA approved for the treatment of skin and soft tissue infections.
mechanism of action Chloramphenicol inhibits protein synthesis in bacteria, and to a lesser extent, in eukaryotic cells. It binds reversibly to the 50S ribosomal subunit (near the binding site for the macrolide antibiotics and clindamycin). The drug prevents the binding of the amino acid-containing end of the aminoacyl tRNA to the acceptor site on the 50S ribosomal subunit. The interaction between peptidyltransferase and its amino acid substrate is blocked, inhibiting peptide bond formation (Figure 46-2).
Chloramphenicol also inhibits protein synthesis in mammalian mitochondria via a similar mechanism, perhaps because their ribosomes somewhat resemble bacterial ribosomes; erythropoi-etic cells are particularly sensitive.
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