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Pharmacology · Antibacterial Chemotherapeutic Agents

Aminoglycosides

Aminoglycosides

Aminoglycosides are a class of highly polar bactericidal antibiotics. They are distinguished by potent activity against gram-negative microorganisms and a specific mechanism of protein synthesis disruption at the ribosomal level.

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Spectrum of activityPredominantly gram-negative aerobes and *Pseudomonas aeruginosa*
TargetIrreversible binding to the 30S ribosomal subunit
EliminationRenal excretion unchanged; nephrotoxic
ToxicityOtotoxicity and risk of neuromuscular blockade
2 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Chemical structure and generations

The core of the molecules is an aminocyclitol cyclic alcohol linked via glycoside bonds to aminosugars. Natural compounds are produced by actinomycetes of the genera Actinomyces and Micromonospora.

Pharmacology distinguishes three generations of drugs:

  • 1st generation: Streptomycin, neomycin, kanamycin.
  • 2nd generation: Gentamicin, tobramycin, netilmicin.
  • 3rd generation: Amikacin (has the broadest spectrum and is resistant to inactivating bacterial enzymes).

Mechanism of transport and action

Antibiotic penetration into the cell occurs in two stages: passive diffusion through porins and energy-dependent active transport across the cytoplasmic membrane. The process critically depends on oxygen availability, which is why the drugs are ineffective against anaerobes.

Inside the cell, aminoglycosides exert a bactericidal effect:

  1. They bind to the 30S ribosomal subunit.
  2. They cause mistranslation—incorrect reading of the mRNA genetic code.
  3. They trigger the synthesis of defective (aberrant) proteins.
  4. Aberrant proteins incorporate into the membrane, disrupting it and enhancing the penetration of new antibiotic doses.
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Pharmacokinetics and synergism

Being polycations, aminoglycosides are lipophobic, poorly absorbed from the gastrointestinal tract, and not metabolized in the body, being excreted by the kidneys.

An important feature is synergism with beta-lactams: penicillins damage the cell wall, facilitating the transport of aminoglycosides into the bacterium. For example, the combination of gentamicin with benzylpenicillin is effective in severe enterococcal infections.

Side effects and limitations

Systemic administration of the drugs requires strict monitoring due to severe adverse reactions:

  • Pronounced ototoxicity (damage to hearing and the vestibular apparatus).
  • Nephrotoxicity (kidney damage).
  • Risk of neuromuscular blockade, which can cause respiratory depression.
  • Contraindications include pregnancy, myasthenia gravis, renal pathologies, and auditory nerve pathologies.
How to memorize

A-mino-GLY-co-sides — DEAF-ness and TWIN-neys (kidneys suffer alongside hearing, and the drugs work "in pairs" with beta-lactams).

Class and exam questions

Why are aminoglycosides ineffective in anaerobic conditions and purulent foci?

Active transport of the antibiotic across the cytoplasmic membrane is an energy- and oxygen-dependent process. In oxygen-depleted anaerobic conditions, as well as in acidic or hyperosmolar environments, transport is blocked.

Why can't aminoglycosides and beta-lactams be mixed in the same syringe?

They have opposite charges: aminoglycosides are positively charged, while penicillins are negatively charged. When administered together, they form an inactive precipitate and lose antimicrobial activity.

What is the main advantage of amikacin over 2nd-generation drugs?

Amikacin belongs to the 3rd generation and has the broadest spectrum. It is not degraded by bacterial enzymes that inactivate gentamicin and tobramycin, making it effective against multidrug-resistant strains.

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What else to study on this topic

  • Features of neomycin and kanamycin use for local therapy and intestinal decontamination
  • Pharmacokinetic properties of netilmicin and its chemical protection against enzymes
  • The role of divalent cations (including calcium in bone tissue) in reducing drug activity
  • Clinical indications and limitations for 1st-generation drugs in tuberculosis and particularly dangerous infections
  • Mechanism of neuromuscular blockade development and approaches to its prevention

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Other topics in the section "Antibacterial Chemotherapeutic Agents"

Bacterial protein synthesis: targets for antibioticsPeptidoglycan synthesis (bacterial cell wall)Classification of antibioticsSulfonamidesUrinary antiseptics and intestinal antisepticsAntituberculosis drugsSelection of antimicrobial therapy by pathogenMechanisms of antibiotic actionMicrobial resistanceBeta-lactam antibioticsNatural penicillinsSemisynthetic penicillinsAntipseudomonal penicillinsBeta-lactamase inhibitor-protected penicillinsCephalosporinsFourth-generation cephalosporinsBeta-lactamase inhibitor-protected cephalosporinsCarbapenemsMonobactamsFosfomycinCycloserineBacitracinAntibiotics that inhibit protein synthesisMacrolides
Entire section "Antibacterial Chemotherapeutic Agents"

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