Lecture on Antibiotics: Protein Synthesis Inhibitors
Overview
- Transition from cell wall inhibitors to protein synthesis inhibitors in antibiotics.
- Focus on ribosomes:
- Bacteria have 70s ribosomes.
- Eukaryotic cells have 80s ribosomes.
- Mitochondria in human cells also contain 70s ribosomes, leading to potential mitochondrial concerns.
Key Characteristics of Protein Synthesis Inhibitors
- Generally broad-spectrum antibiotics.
- Often bacteriostatic, slowing growth rather than killing bacteria. However, some can be bactericidal at high doses or in combination.
- More effective against a wide range of bacteria compared to cell wall inhibitors.
Major Classes of Protein Synthesis Inhibitors
Chloramphenicol, Macrolides, Lincomycins
- Bind to the 50s large subunit of ribosomes.
- Prevent peptide bond formation, stopping protein synthesis.
Aminoglycosides
- Focus of the lecture.
- Bind to the 30s subunit, causing codon-anticodon mismatches.
- Lead to insertion of wrong amino acids, creating faulty proteins that disrupt cytoplasmic membranes.
- Broad-spectrum and bactericidal.
Examples of Aminoglycosides
-
Streptomycin
- Broad-spectrum.
- Historically cheap and widely used, leading to resistance.
- Effective against Mycobacterium tuberculosis and Mycobacterium leprae.
-
Gentamicin
- Broad-spectrum.
- Effective against Pseudomonas infections.
- Important for treating infections in cystic fibrosis patients.
-
Neomycin
- Used topically, such as in Neosporin.
Usage Concerns
- Toxicity
- Nephrotoxic (affects kidneys).
- Neurotoxic (affects nervous system, possible ear damage).
- Risk of use evaluated against severity of infection (e.g., CF patients with Pseudomonas or TB).
Conclusion
- Introduction to protein synthesis inhibitors, beginning with aminoglycosides.
- Importance of weighing risks and benefits due to possible side effects.
Note: This is an introductory segment on protein synthesis inhibitors; subsequent lectures will cover additional details and other antibiotic classes.