mitoquinone and Tendinopathy

Tendinitis and tendon rupture during treatment with fluoroquinolone antibiotics is thought to be mediated via oxidative stress. This study investigated whether ciprofloxacin and moxifloxacin cause oxidative stress and mitochondrial damage in cultured normal human Achilles' tendon cells and whether an antioxidant targeted to mitochondria (MitoQ) would protect against such damage better than a non-mitochondria targeted antioxidant. Human tendon cells from normal Achilles' tendons were exposed to 0-0.3 mM antibiotic for 24 h and 7 days in the presence of 1 microM MitoQ or an untargeted form, idebenone. Both moxifloxacin and ciprofloxacin resulted in up to a 3-fold increase in the rate of oxidation of dichlorodihydrofluorescein, a marker of general oxidative stress in tenocytes (p<0.0001) and loss of mitochondrial membrane permeability (p<0.001). In cells treated with MitoQ the oxidative stress was less and mitochondrial membrane potential was maintained. Mitochondrial damage to tenocytes during fluoroquinolone treatment may be involved in tendinitis and tendon rupture.

Topics: Achilles Tendon; Anti-Infective Agents; Antioxidants; Aza Compounds; Cell Survival; Cells, Cultured; Ciprofloxacin; Fluoroquinolones; Humans; Intracellular Membranes; Membrane Potential, Mitochondrial; Mitochondria; Moxifloxacin; Organophosphorus Compounds; Oxidative Stress; Quinolines; Rupture; Tendinopathy; Ubiquinone