Ciprofloxacin-Induced Oxidative Stress Promotes a Senescence-like Phenotype in Human Fibroblasts In Vitro
Abstract
Fluoroquinolones are effective synthetic broad-spectrum antibiotics, but their use can be associated with persistent adverse effects, sometimes described as fluoroquinolone-induced disability. The molecular mechanisms underlying these effects remain incompletely understood, although accumulating evidence implicates mitochondrial dysfunction, oxidative stress, and DNA damage. We hypothesized that the convergence of these stress responses may promote cellular senescence and thereby contribute to persistent fluoroquinolone-associated adverse effects. We examined three clinically used fluoroquinolones-ciprofloxacin, moxifloxacin, and levofloxacin-in primary human fibroblasts in vitro. Exposure for 7 days revealed that 200 µM ciprofloxacin, but not 200 µM moxifloxacin or 500 µM levofloxacin, induced a senescence-like phenotype characterized by increased senescence-associated β-galactosidase (SA-β-Gal) activity and an elevated senescence index (SI), which integrates increased cell size and autofluorescence measured by imaging flow cytometry. At 7 days, ciprofloxacin did not induce a broad canonical senescence-associated secretory phenotype (SASP) at either the transcriptional or secretory level, consistent with a non-canonical senescence-like state; only a modest increase in IL-1β secretion emerged after 14 days. The ciprofloxacin-induced phenotype was not accompanied by a robust increase in the canonical p53, p16, or p21 protein markers, but was associated with reduced…
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