Aminoglycosides have a specific mechanism that affects which stage of translation?

Aminoglycosides, such as gentamicin and tobramycin, have a unique mechanism of action that primarily induces premature termination or mistranslation during protein synthesis. They bind to the 30S ribosomal subunit, causing misreading of the mRNA. This misreading can lead to the incorporation of incorrect amino acids into the growing polypeptide chain, which disrupts the function of the resultant protein. In some cases, this binding can also lead to premature termination of the translation process altogether, resulting in truncated proteins.

The mechanism highlights the critical role of proper translation fidelity in maintaining cell function. By interfering with accurate translation, aminoglycosides can effectively inhibit bacterial protein synthesis, exerting their bactericidal effects. This action is particularly significant in the treatment of serious infections caused by Gram-negative bacteria.

Other options describe different interactions with the ribosome or processes involved in protein synthesis and transcription, but they do not accurately represent the specific action of aminoglycosides. For example, inhibiting translocation plays a role for some antibiotics like macrolides and tetracyclines, while blocking tRNA binding typically pertains to other classes of antibacterials such as chloramphenicol or linezolid. Additionally, inhib