Mechanism of action<unk>  inhibits protein synthesis by blocking the attachment of charged tRNA at the P site peptide chain.<unk>  blocks the A-site so that a hydrogen bond is not formed between the amino acids.<unk>  binds to the 30S and 50S subunit of microbial ribosomes. Thus, it prevents the formation of a peptide chain. The action is usually not inhibitory and irreversible even with the withdrawal of the drug. Mammalian cells are less vulnerable to the effect of<unk> s, despite the fact that<unk>  binds to the small ribosomal subunit of both prokaryotes and eukaryotes (30S and 40S, respectively). This is because bacteria actively pump<unk>  in, even against a concentration gradient, whereas mammalian cells are simply not affected by the mechanisms of<unk>  within the cytoplasm. This accounts for the relatively small off-site effect of<unk>  on human cells. Mechanisms of resistance Bacteria usually acquire resistance to<unk>  from horizontal transfer of a gene that either encodes an efflux pump or a ribosomal protection protein. Efflux pumps actively eject<unk>  from the cell, preventing the buildup of an inhibitory concentration of<unk>  in the cytoplasm. Ribosomal protection proteins interact with the ribosome and dislodge<unk>  from the ribosome, allowing for translation to continue.
Tetracycline
Minocycline
Chloramphenicol
Oxytetracycline
Cephalosporin
Anisomycin
Methicillin
Thiamphenicol