Effect of Palosein (superoxide dismutase) and catalase upon oxygen derived free radical induced degradation of equine synovial fluid

Summary The effect of oxygen derived free radicals (ODFR) upon the specific viscosity of equine synovial fluid was studied. ODFR were generated either by a mixture of ferrous iron and EDTA (Fe/EDTA) or by a mixture of hypoxanthine and xanthine oxidase (HX/XO). Incubation of the synovial fluid with both free radical generating systems decreased its specific viscosity. When the synovial fluid was incubated with Fe/EDTA the specific viscosity of the synovial fluid was reduced rapidly. By 2 mins, it was 53±3 per cent of the original specific viscosity and by 30 mins it was reduced to 39±5 per cent. In the HX/XO system, the specific viscosity was 75±4 per cent of the original specific viscosity at 10 mins and by 50 mins it was reduced to 55±3 per cent. Palosein (superoxide dismutase) was an effective inhibitor of the free radical induced reduction of the viscosity of the synovial fluid when the free radicals were generated with HX/XO but not with Fe/EDTA. Catalase was moderately effective as an inhibitor of reduction in specific viscosity of the synovial fluid when the free radicals were generated by either system. Only minor synergy resulted when mixtures of Palosein and catalase were tested for inhibition of Fe/EDTA induced reduction in the specific viscosity of equine synovial fluid. The results indicate that Palosein may protect equine synovial fluid from the effects of the superoxide radical (0 2 − ) but not from the hydroxyl radical (OH*). It was suggested that catalase may be a more appropriate antioxidant for the treatment of inflammatory disorders of the joint because it provided moderate protection from both ODFR producing systems. In addition, it was suggested that Palosein will not directly protect equine synovial fluid in vivo against ODFR generated by iron in the absence of superoxide, although it may provide protection through a secondary role by inhibiting mobilisation of iron and the reduction of ferric ions in vivo.