Oxidative stress is involved in the pathogenesis of diabetes. We have proposed Xanthine Oxidase as an enzymatic mechanism to explain the increased generation of free radicals (FR) in diabetes. Recent studies show that there is a redox regulation of cellular signalling and that the generation of FR leads to the activation of MAPKs pathway. This pathway induces the activation of NF-kB which plays an important role in the regulation of gene activity. The purpose of the present study was to test the hypothesis that in streptozotocin induced diabetes, xathine oxidase-derived free radicals, causes an activation of important cell signalling pathways such as MAPKs and NF-kB which leads to the expression of iNOS. Male wistar rats were randomly divided into 3 groups: control, diabetic and diabetic but pretreated with allopurinol (32 mg/kg). .Our results show that that Type I diabetes causes activation of MAPKs, IkB and NF-kB in liver. The inhibition of xanthine oxidase with allopurinol prevents this activation.