Mouse liver oxidative stress caused by chronic protein malnutrition and DEN. Protection by Met

Puerto Madryn. Chubut. Argentina

Congreso; XLVI Reunión Anual - Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; 2010

Many liver diseases are linked to the occurrence of an oxidative stress. Thus, cells have strategies to preserve their redox balance with enzymes such as superoxide dismutase (SOD) and catalase (CAT), and regular amino acid dietary supply. Conversely, diethylnitrosamine (DEN) form electrophilic species responsible for hepatic oxidative stress. This work studied the effect of chronic protein malnutrition on the hepatic oxidative status of mice treated with DEN. Also, we evaluated the action of dietary Met against oxidative stress. Balb/C mice were fed during 5 days with a protein-free diet followed by 5 days of complete diet, repeated 3 times (3PFD-CD). In addition, both the effect of Met supplementation (3PFD+Met-CD) and DEN injection (i) were studied. The oxidative status of liver was evaluated analyzing the activities of SOD and CAT, and the level of protein carbonylation. 3PFD-CD decreased the activities of SOD (-32%) and CAT (-30%) while protein carbonylation increased (+74%). On the other hand, 3PFD-CDi decreased both the activities of SOD (-70%) and the levels of protein carbonylation (-40%). Addition of Met to PFD preserved the normal values in all conditions. In conclusion, 3PFD-CD and DEN act synergically to cause hepatic oxidative stress. Conversely, dietary Met proves to exert a main role on cellular detoxification by decreasing this stress. Supported by CONICET and UNMDP.