Selective toxicity of antibacterial agents-still a valid concept or do we miss chances and ignore risks?
Level 5 - mechanism / opinion, no new human data
Narrative review of biological mechanisms with no original human empirical data or systematic review methodology.
PubMed 33367978 · doi:10.1007/s15010-020-01536-y
What was done
This narrative review synthesized literature describing the multiple molecular modes of action of antibacterial drug classes on eukaryotic cells and pathways, evaluating the validity and limitations of the classical concept of selective toxicity.
What was found
The abstract reports no quantitative values or statistical metrics. It qualitatively details multiple eukaryotic pathways affected by antibiotics: - Aminoglycosides, macrolides, oxazolidinones, chloramphenicol, clindamycin, tetracyclines, glycylcyclines, fluoroquinolones, rifampicin, bedaquiline, and beta-lactams inhibit mitochondrial translation through mitosome binding or inhibition of mitochondrial RNA polymerase, topoisomerase 2β, ATP synthesis, or transporter activities. - Oxazolidinones, tetracyclines, vancomycin, beta-lactams, bacitracin, isoniazid, and nitroxoline inhibit matrix metalloproteinases (MMPs) via zinc and calcium chelation, whereas fluoroquinolones and chloramphenicol chelate these cations but increase MMP activities. - Aminoglycosides, macrolides, chloramphenicol, oxazolidinones, and tetracyclines induce read-through of premature stop codons. - Other noted targets include fluoroquinolone interaction with eukaryotic DNA damage repair and oxazolidinone inhibition of mucin overproduction.
Why it matters
It highlights that mammalian host-cell interactions are intrinsic to many antibiotic classes due to evolutionary target homologies, explaining potential mechanistic pathways for adverse drug effects and off-target clinical actions.
Limits
The review is non-systematic, providing no formal search criteria, study selection protocol, or risk-of-bias grading. The abstract provides no quantitative effect sizes, dosing thresholds, or human clinical trial outcomes.
Cited by
- supports Certain classes of antibiotics can induce stress in human mitochondria because mitochondria retain bacterial-derived enzymes due to their bacterial evolutionary origin.