Modification of oxidative stress in response to intestinal preconditioning

Previous studies have demonstrated that intestinal preconditioning protects the organ from ischemia reperfusion damage. Xanthine oxidase mediating fre e radical generation contributes to the development of injury associated to l ischemia reperfusion, Thus, any process able to modulate the oxygen free radical generation system could attenuate the injury. Also, it is known tha t nitric oxide is implicated in the preconditioning response. The aim of th is work is to determine: (1) the effect of intestinal preconditioning on th e xanthine oxidase system, (2) the relevance of this system in the developm ent of injury, and (3) its relationship with nitric oxide. For this purpose , we have determined the activity of the xanthine dehydrogenase/xanthine ox idase system, th! levels of its substrate (xanthine), and end-product (uric acid) and oxidant stress status in rat small intestine subjected to ischem ic preconditioning. The effects of nitric oxide inhibition have also been e valuated. Results show that the percentage of xanthine dehydrogenase to xan thine oxidase conversion, xanthine, uric acid concentration, lipoperoxides, and reduced glutathione were significantly reduced in preconditioned rats irrespectively of nitric oxide inhibition. In summary, this work shows that oxidative stress in intestinal preconditioning is reduced as consequence o f the diminished conversion of xanthine dehydrogenase to xanthine oxidase, and also as a consequence of the reduced availability of xanthine.