Model Answer
0 min readIntroduction
Protein synthesis is a fundamental process in all living organisms, but significant differences exist between prokaryotic and eukaryotic systems, making it a prime target for antimicrobial agents. Antibiotics and certain toxins exploit these differences to selectively inhibit protein synthesis, leading to cell death or growth inhibition. Understanding these mechanisms is crucial for developing effective therapies and combating antibiotic resistance. This answer will detail the antibiotics and toxins that inhibit protein synthesis in both prokaryotes and eukaryotes, along with a brief explanation of their respective mechanisms of action.
Antibiotics Inhibiting Prokaryotic Protein Synthesis
Prokaryotic protein synthesis is a major target for antibiotics due to the structural differences between prokaryotic (70S) and eukaryotic (80S) ribosomes. Several classes of antibiotics interfere with different stages of this process.
1. Aminoglycosides (e.g., Streptomycin, Gentamicin)
- Mechanism: Bind to the 30S ribosomal subunit, causing misreading of mRNA and premature termination of translation. They also interfere with the initiation complex formation.
- Prokaryotes: Highly effective due to the higher affinity for the 70S ribosome.
- Eukaryotes: Lower affinity for the 80S ribosome, resulting in less toxicity, but some mitochondrial toxicity can occur.
2. Tetracyclines (e.g., Doxycycline, Minocycline)
- Mechanism: Bind to the 30S ribosomal subunit, preventing the attachment of aminoacyl-tRNA to the A-site of the ribosome, thus blocking the addition of amino acids to the growing polypeptide chain.
- Prokaryotes: Effectively inhibit bacterial growth.
- Eukaryotes: Can inhibit protein synthesis in eukaryotic cells, but uptake is generally limited, reducing toxicity.
3. Macrolides (e.g., Erythromycin, Azithromycin)
- Mechanism: Bind to the 23S rRNA of the 50S ribosomal subunit, blocking the translocation step of protein synthesis – the movement of the ribosome along the mRNA.
- Prokaryotes: Widely used against bacterial infections.
- Eukaryotes: Can bind to the 50S subunit of eukaryotic ribosomes, but with lower affinity, leading to some side effects.
4. Chloramphenicol
- Mechanism: Binds to the 23S rRNA of the 50S ribosomal subunit, inhibiting peptidyl transferase activity, preventing peptide bond formation.
- Prokaryotes: Broad-spectrum antibiotic.
- Eukaryotes: Can inhibit mitochondrial protein synthesis (as mitochondria have 70S-like ribosomes), leading to bone marrow suppression.
5. Lincosamides (e.g., Clindamycin)
- Mechanism: Similar to macrolides, bind to the 23S rRNA of the 50S ribosomal subunit, inhibiting translocation.
- Prokaryotes: Effective against many Gram-positive bacteria.
- Eukaryotes: Similar to macrolides, lower affinity for eukaryotic ribosomes.
Toxins Inhibiting Protein Synthesis
1. Diphtheria Toxin
- Mechanism: Inhibits elongation factor 2 (EF-2), a GTP-dependent factor essential for translocation. This prevents the movement of tRNA from the A-site to the P-site.
- Prokaryotes & Eukaryotes: Affects both, but its primary effect in humans is on eukaryotic cells.
2. Shiga Toxin (produced by *Shigella dysenteriae*)
- Mechanism: Cleaves 28S rRNA in the 60S ribosomal subunit, inhibiting protein synthesis.
- Prokaryotes & Eukaryotes: Affects both, but its primary effect in humans is on eukaryotic cells, causing hemorrhagic colitis and hemolytic uremic syndrome.
Comparison Table
| Inhibitor | Target | Mechanism | Prokaryotes | Eukaryotes |
|---|---|---|---|---|
| Streptomycin | 30S Ribosome | Misreading of mRNA | High | Low (some mitochondrial toxicity) |
| Tetracycline | 30S Ribosome | Blocks tRNA attachment | High | Low |
| Erythromycin | 50S Ribosome | Blocks translocation | High | Low |
| Chloramphenicol | 50S Ribosome | Inhibits peptidyl transferase | High | Moderate (mitochondrial toxicity) |
| Diphtheria Toxin | EF-2 | Inhibits translocation | Both | Primary effect on eukaryotic cells |
| Shiga Toxin | 28S rRNA | Cleaves rRNA | Both | Primary effect on eukaryotic cells |
Conclusion
In conclusion, a diverse range of antibiotics and toxins target protein synthesis in prokaryotes and eukaryotes, exploiting structural and functional differences in their ribosomal machinery. While many antibiotics selectively target bacterial ribosomes, some exhibit toxicity towards eukaryotic cells, particularly affecting mitochondrial function. Understanding these mechanisms is vital for developing new antimicrobial strategies and minimizing adverse effects. The emergence of antibiotic resistance necessitates continuous research into novel inhibitors of protein synthesis.
Answer Length
This is a comprehensive model answer for learning purposes and may exceed the word limit. In the exam, always adhere to the prescribed word count.