The antibacterial actions of the aminoglycosides involve two possibly synergistic effects. First, the positively charged aminoglycoside binds to negatively charged sites on the outer bacterial membrane, thereby disrupting membrane integrity. It is likely that the aminoglycoside-induced bacterial outer membrane degradation accounts for the rapid concentration-dependent bactericidal effect of these compounds. Second, aminoglycosides bind to various sites on bacterial 30S ribosomal subunits, disrupting the initiation of protein synthesis and inducing errors in the translation of messenger RNA to peptides. They also bind to sites on bacterial 50S ribosomal subunits, although the significance of this binding is uncertain. In addition, they have a postantibiotic effect; that is, they continue to suppress bacterial regrowth even after removal of the antibiotic from the bacterial microenvironment. It is likely that ribosome disruption accounts for this postantibi-otic activity.
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