Ciprofloxacin and a senescence-like phenotype in human fibroblasts in vitro
In cultured human fibroblasts, 7-day exposure to 200 µM ciprofloxacin, but not moxifloxacin or levofloxacin, produced a senescence-like phenotype; antioxidants reduced it, and the signal recovered after drug removal. [1]
Automatic summary · not editorially reviewed
The key findings
After 7 days, 200 µM ciprofloxacin, but not 200 µM moxifloxacin or 500 µM levofloxacin, induced a senescence-like phenotype in primary human fibroblasts in vitro. [1]
The phenotype lacked a broad canonical secretory program at 7 days and robust increases in p53, p16 or p21, but was associated with reduced RB phosphorylation at Ser795. [1]
Trolox and the mitochondria-targeted antioxidant SkQ3 attenuated the ciprofloxacin-induced increase in SA-β-Gal activity and senescence index, and the resazurin signal recovered after drug removal. [1]
The source at a glance
- Study type / format
- In vitro laboratory study (abstract)
- Population / context
- Primary human fibroblasts in vitro
- Summary based on
- Study abstract
- Original publication
- September 29, 2026
Fibroblasts tested with three fluoroquinolones
The authors asked whether stress responses to fluoroquinolones could promote cellular senescence and so contribute to persistent adverse effects. They exposed primary human fibroblasts in vitro to three clinically used fluoroquinolones: ciprofloxacin, moxifloxacin and levofloxacin. After 7 days, 200 µM ciprofloxacin, but not 200 µM moxifloxacin or 500 µM levofloxacin, induced a senescence-like phenotype. This was shown by increased senescence-associated β-galactosidase activity and an elevated senescence index combining cell size and autofluorescence.
Supporting source [1]
Non-canonical markers and antioxidant attenuation
At 7 days, ciprofloxacin did not induce a broad canonical senescence-associated secretory phenotype at transcriptional or secretory level; only a modest rise in IL-1β secretion appeared after 14 days. The phenotype was not accompanied by a robust increase in the canonical p53, p16 or p21 protein markers, but was associated with reduced RB phosphorylation at Ser795. Ciprofloxacin also increased oxidative stress. Both the antioxidant Trolox and the mitochondria-targeted antioxidant SkQ3 attenuated the ciprofloxacin-induced increase in SA-β-Gal activity and senescence index.
Supporting source [1]
Recovery after ciprofloxacin removal in culture
When ciprofloxacin was removed from the culture medium after 1 or 2 weeks of incubation, the resazurin signal recovered to approximately control values by the end of the 3-week experimental period. The authors describe oxidative stress as a putative mediator of ciprofloxacin-induced senescence-like remodeling in human fibroblasts and support further investigation of drug-induced cellular senescence as a potential contributor to persistent fluoroquinolone-associated adverse effects. These are in vitro findings in fibroblasts; they do not show effects on human lifespan or establish that the drug causes persistent harm in people.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from primary human fibroblasts in vitro, not from people, and do not establish persistent adverse effects or any effect on human lifespan.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Kondratenko ND, Chelombitko MA, Zinovkina LA, Dashkevich AA, Prikhodko AS, Kuptsova RY, Ziubina EP, Lyamzaev KG, Zinovkin RA. · europepmc.org · September 29, 2026