Chloramphenicol blocks proper binding of 50S site which, stops protein synthesis. It does inhibit mitochondrial ribosomal protein synthesis because these ribosomes are 70S, the same as those in bacteria. It does not bind to the 80S mammalian ribosomes. This may be responsible for the dose related anemia caused by chloramphenicol.
Macrolides, clindamycin, prevent transfer of the growing polypeptide chain within the 50S site so a new charged tRNA cannot bind to the ribosome so, stops protein synthesis.
Tetracyclines bind to 30S ribosomal subunit at a site that blocks binding of charged tRNA to the 50S site of the ribosome. Tetracyclines can inhibit mammalian protein synthesis, but because they are “pumped” out of most mammalian cells do not usually reach concentrations needed to significantly reduce mammalian protein synthesis.
Aminoglycosides: Protein synthesis is inhibited by aminoglycosides in at least three ways: (1) They interfere with the “initiation complex” of peptide formation; (2) they induce misreading of mRNA, which causes incorporation of incorrect amino acids into the peptide, resulting in a non- functional or toxic protein; and (3) they cause a breakup of polysomes into nonfunctional monosomes. These activities occur more or less simultaneously, and the overall effect is irreversible and lethal for the cell.
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