Hindawi Publishing Corporation Experimental Diabetes Research Volume 2011, Article ID 754132, 6 pages doi:10.1155/2011/754132 Research Article Exogenous Superoxide Dismutase: Action on Liver Oxidative Stress in Animals with Streptozotocin-Induced Diabetes F´ abio Cangeri Di Naso, 1 Alexandre Sim˜ oes Dias, 1, 2 Marilene Porawski, 1, 3 and Norma Anair Possa Marroni 1, 4 1 Laboratory of Experimental Hepatology and Physiology, Hospital de Cl´ ınicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, 90050-170 Porto Alegre, RS, Brazil 2 School of Physical Education, Physical Therapy Course, Federal University of Rio Grande do Sul 90690-200, Porto Alegre , RS, Brazil 3 Pontif´ ıcia Universidade Cat´ olica do Rio Grande do Sul (PUCRS), 91530-000 Porto Alegre, RS, Brazil 4 Universidade Luterana do Brasil, 92120-015 Canoas, RS, Brazil Correspondence should be addressed to F´ abio Cangeri Di Naso, fdinaso@yahoo.com.br Received 22 September 2010; Revised 14 December 2010; Accepted 4 January 2011 Academic Editor: Subrata K. Chakrabarti Copyright © 2011 F´ abio Cangeri Di Naso et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Aim. To investigate the effects of exogenous antioxidant copper zinc superoxide dismutase (Cu/Zn SOD) on oxidative stress in the experimental model of diabetes mellitus (DM). Methods. Twenty eight male Wistar rats divided in four groups were used: control (CO), controls treated with SOD (CO + SOD), diabetics (DM), and diabetics treated with SOD (DM + SOD). SOD (orgotein, 13 mg/Kg body weight was administered. DM was induced by a single streptozotocin injection (i.p., 70 mg/kg), and 60 days later, we evaluated liver oxidative stress. Results. Liver lipoperoxidation was increased in the DM group and significantly decreased in the DM + SOD group. Nitrite and nitrate measures were reduced in the DM and increased in the DM + SOD group, while iNOS expression in the DM group was 32% greater than in the CO and 53% greater in the DM + SOD group than in the DM group (P<.01). P65 expression was 37% higher in the DM (P<.05), and there was no significant difference between the DM and DM + SOD groups. Conclusion. SOD treatment reduced liver oxidative stress in diabetic animals, even though it did not change NFκB. SOD also increased NO, probably by the increased dismutation of the superoxide radical. The iNOS expression increase, which became even more evident after SOD administration. 1. Introduction Diabetes mellitus (DM) is an endocrine-metabolic disorder of increasing incidence and clinical relevance, contributing to high morbidity and mortality rates [1]. Due to population aging, urbanization, increased prevalence of obesity, and physical inactivity, the number of individuals affected by DM is increasing in many parts of the world [2]. In view of this growing incidence, the study of the physiological routes of DM becomes crucial for the emergence of novel therapeutic procedures [3]. Four physiopathological pathways are involved and cause the chronic complications of the disease: the polyols pathway, protein kinase C activation, increase in the hexosamine flow rate, and the advanced glycation end-products (AGE) pathway. Although the disorder presents different routes of activation, oxidative stress (OE) is present in all the above- mentioned pathways. Strategies to reduce the formation of superoxide anion (O − ·) and thus oxidative stress are relevant to the treatment of DM [4]. The action of O − · scavengers is performed by a group of antioxidant enzymes called superoxide dis- mutases (SODs), which catalyze the dismutation of O − · into hydrogen peroxide (H 2 O 2 ) and oxygen (O 2 )efficiently and specifically. Mammal tissues have 3 SODs isoforms: Cu/Zn superoxide dismutase (SOD1), Mn SOD (SOD2), and extracellular SOD (EC-SOD, or SOD3). SOD1 is a 32kDA homodimer cell protein containing copper and zinc, and