Abatement by naringin of lomefloxacin-induced genomic instability in mice

Lomefloxacin is a difluorinated quinolone antibacterial drug. It is widely used against infectious diseases including meningitis, those of the genitourinary and upper respiratory tracts, and skin infections. Lomefloxacin, like other fluoroquinolones, is mutagenic and the formation of reactive oxygen species appears to be responsible for this genomic instability. The anti-mutagenic effects of naringin, a grapefruit flavonone, against lomefloxacin-induced genomic instability in vivo were evaluated in mouse bone marrow cells by chromosomal aberration and micronucleus (MN) assays. Naringin was neither genotoxic nor cytotoxic in mice at doses equivalent to 5 or 50 mg/kg. Pre-treatment of mice with naringin significantly reduced lomefloxacin-induced chromosomal aberrations and the MN formation in bone marrow. The protective effect of naringin was found to be stronger at the higher dose, indicating the dose-dependent effect of naringin. Lomefloxacin induced marked biochemical alterations characteristic of oxidative stress, including enhanced lipid peroxidation and reduction in the reduced glutathione level. Prior administration of naringin ahead of lomefloxacin challenge ameliorated these biochemical markers. It is concluded that naringin has a protective role in the abatement of lomefloxacin-induced genomic instability that resides, at least in part, in its anti-radical effects. Thus, naringin might be a good alternative to reduce genotoxic risks associated with lomefloxacin therapy.