Oxygen-derived free radical damage in organ preservation: activity of superoxide dismutase and xanthine oxidase.

It has been suggested that the generation of oxygen-derived free radicals during the reperfusion of injured tissue causes organ dysfunction. The mechanism apparently involves the xanthine oxidase (XOD) enzyme system, which becomes activated during reperfusion and generates oxygen-derived free radicals faster than their dismutation by naturally occurring superoxide dismutase (SOD). In this study, we measured the XOD and SOD activities of liver and kidney tissue in species used for organ preservation studies (rats, dogs, and human beings). We also measured the effect that up to 5 days of hypothermic preservation has on the activity of SOD and XOD in canine kidneys and expressed activities as the ratio of SOD to XOD; large ratios suggest lower susceptibility to oxygen-derived free radical damage. The SOD:XOD ratios for rat tissue were consistently lower (kidney = 2.7 X 10(4), liver = 8.9 X 10(3)) than for canine tissue (kidney = 7.0 X 10(5), liver = 4.1 X 10(4)) and human tissue (kidney = 1.1 X 10(6), liver = 6.4 X 10(5)). Canine kidneys perfused for 3 days showed no change in SOD:XOD ratio. After 5 days of perfusion, the SOD:XOD ratio decreased by 50% but was still quite large (5 X 10(5]. This high SOD:XOD ratio in canine and human tissues suggests that they may be less sensitive to oxygen-derived free radical damage than rat tissues.