Bactericidal antibiotics induce mitochondrial dysfunction and oxidative damage in Mammalian cells.
Level 5 - mechanism / opinion, no new human data
Preclinical bench and animal study without human clinical data.
PubMed 23825301 · doi:10.1126/scitranslmed.3006055
What was done
The authors evaluated the mechanistic effects of clinically relevant doses of bactericidal antibiotics (quinolones, aminoglycosides, and β-lactams) versus bacteriostatic antibiotics on mammalian cells in vitro and in vivo in mouse models. They assessed mitochondrial function, reactive oxygen species (ROS) generation, oxidative damage markers (DNA, proteins, and membrane lipids), blood markers, and antioxidant defense gene expression in mice. They also tested whether co-administration of the antioxidant N-acetyl-L-cysteine (NAC) mitigated these effects.
What was found
The abstract reports no numerical values. Bactericidal antibiotics caused mitochondrial dysfunction, ROS overproduction, and oxidative damage to DNA, proteins, and membrane lipids in mammalian cells. Mice treated with bactericidal antibiotics exhibited elevated blood markers of oxidative stress, oxidative tissue damage, and upregulation of antioxidant defense genes. These deleterious effects were alleviated in cell culture and in mice by administering N-acetyl-L-cysteine or prevented by using bacteriostatic antibiotics.
Why it matters
This study identifies mitochondrial dysfunction and oxidative stress as a common mechanism underlying mammalian adverse effects from major classes of bactericidal antibiotics. It suggests that antioxidant co-therapy or selecting bacteriostatic alternatives could potentially mitigate antibiotic-induced tissue toxicities.
Limits
The abstract reports no quantitative values, sample sizes, or specific dosing regimens. The study is entirely preclinical (in vitro mammalian cell culture and mouse models) and does not provide clinical data or evaluate patient 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.