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Ofloxacin, a quinolone, is an extensively used, well-tolerated antibacterial agent but has been reported to induce photosensitivity at low incidences. In the present investigation, the possible role of oxidative stress in ofloxacin-induced retinopathy in rabbits was evaluated. It was observed that ofloxacin at a dose rate of 10 and 20 mg/rabbit, twice daily for 21 consecutive days, resulted in significant elevation in the extent of lipid peroxidation and depletion of the blood glutathione levels. Marked alterations were also observed in various parameters of the glutathione-redox cycle. There was significant increase in the enzymic activity of glutathione peroxidase and glutathione reductase, whereas a significant decrease was observed in the activities of superoxide dismutase, catalase, and glutathione-S-transferase enzymes. Histopathological studies revealed retinal damage especially in the pigmented cell layer. Degenerative changes in liver and kidneys were also observed. Liver showed focal areas of necrosis, dilation of sinusoids, and cellular infiltration, whereas in kidneys, there was glomerular and tubular degeneration, suggesting impaired renal functioning.

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The effect of 21 days of repeated oral administration of levofloxacin and enrofloxacin both alone and in combination with meloxicam, on the oxidative balance in blood was evaluated in rabbits. Rabbits were randomly allocated to six groups of four animals each. Control group was gavaged 5% dextrose and 2% benzyl alcohol. Three groups were exclusively gavaged meloxicam (0.2 mg/kg body weight o.d.), levofloxacin hemihydrate (10 mg/kg body weight b.i.d 12 h), and enrofloxacin (20 mg/kg body weight o.d.), respectively. Two other groups were co-gavaged meloxicam with levofloxacin hemihydrate and enrofloxacin, respectively. A reduction ( p < 0.05) of reduced glutathione levels was observed in groups treated with meloxicam both alone and in combination with levofloxacin, whereas an increase ( p < 0.01) in the levels of this antioxidant was observed in the groups treated with enrofloxacin. The activities of enzymes, glutathione peroxidase and superoxide dismutase, were induced ( p < 0.05) in levofloxacin-alone treated group. Superoxide dismutase was also induced ( p < 0.05) in meloxicam-alone treated group and inhibited ( p < 0.05) in enrofloxacin-meloxicam co-treated group. The activity of catalase was non-significantly different between various groups. Enrofloxacin-treated groups had higher ( p < 0.01) lipid peroxidation than control and levofloxacin-alone treated groups. Elevated lipid peroxidation was also observed in the groups treated with meloxicam both alone and in combination with levofloxacin ( p < 0.05). In conclusion, these drugs have potential to induce oxidative imbalance, however, compared to levofloxacin, more oxidative damage is produced by enrofloxacin and meloxicam.