Selective toxicity in antimicrobial therapy: The most selectively toxic antibacterial agents are those that inhibit the synthesis of which unique bacterial structure?

Introduction / Context:
Selective toxicity is the key principle behind antimicrobial chemotherapy. Drugs that target structures absent in humans typically offer the best safety margins.

Given Data / Assumptions:

• Mammalian cells lack peptidoglycan cell walls.
• Several drug targets are listed: DNA, RNA, cell wall, membranes.

Concept / Approach:
Human (eukaryotic) cells do not have peptidoglycan. Therefore, antibiotics that block peptidoglycan biosynthesis (e.g., beta-lactams, glycopeptides) are highly selective for bacteria. By contrast, targeting DNA/RNA or membranes risks off-target effects because eukaryotic cells also rely on these processes, even if bacterial enzymes differ somewhat.

Step-by-Step Solution:
Identify unique bacterial feature: peptidoglycan cell wall. Recall mechanisms: beta-lactams inhibit transpeptidation; glycopeptides inhibit transglycosylation/transpeptidation. Conclude that inhibiting cell wall synthesis provides the greatest selective toxicity.

Verification / Alternative check:
Clinical safety profiles of penicillins and cephalosporins reflect high selectivity; their dose-limiting toxicities are often hypersensitivity rather than direct cytotoxicity to human cells.

Why Other Options Are Wrong:

• Bacterial DNA or RNA synthesis: targets exist (e.g., fluoroquinolones, rifamycins) but eukaryotes possess analogous pathways, so selectivity is less absolute.
• Plasma membranes: differences exist (ergosterol vs. cholesterol in fungi), but bacterial membranes share phospholipid bilayers and are less uniquely targetable than peptidoglycan.

Common Pitfalls:
Confusing “effective” with “selective.” Some highly effective agents are less selective and may carry more host toxicity.

Final Answer:
Bacterial cell walls (peptidoglycan synthesis)