What is the mechanism of action of aminoglycosides?

Aminoglycosides exert their bactericidal effect by binding to ribosomal RNA, which inhibits protein synthesis. They specifically target the 30S subunit of the bacterial ribosome, leading to the misreading of mRNA and the production of nonfunctional or toxic peptides. This disruption in protein synthesis is critical, as proteins are essential for various cellular processes, including enzymatic reactions, structural functions, and the overall survival of the bacteria.

The effectiveness of aminoglycosides in treating infections arises from this mechanism, particularly against aerobic gram-negative bacilli and some gram-positive organisms. The ability of these antibiotics to penetrate bacterial cells and their interaction with ribosomes highlight their role in modern antibiotic therapy, especially for serious infections where rapid bacterial killing is desired.

In contrast, other mechanisms listed in the choices are associated with different classes of antibiotics. For example, disrupting cell membrane integrity is a characteristic of some lipopeptides and polymyxins; inhibiting bacterial cell wall synthesis is primarily the action of beta-lactam antibiotics and glycopeptides; and interference with nucleic acid synthesis is typical of fluoroquinolones and rifamycins. Understanding these distinctions is crucial for selecting the appropriate antibiotic for various bacterial infections.