Deregulation of immune response and oxidative stress contribute to nonalcoholic fatty liver disease (NAFLD) pathogenesis. Resistin is a physiological modulator of inflammation and redox homeostasis of different cell types. Increased resistin serum concentration and the direct association between resistin hepatic expression and NAFLD severity suggest that resistin participates in NAFLD pathogenesis. To evaluate resistin-induced regulation of redox homeostasis in mononuclear leukocytes from NAFLD patients and controls. We evaluated basal and resistin-mediated modulation of reactive oxygen species (ROS) and glutathione content by flow cytometry, and antioxidant enzyme activities by spectrophotometry. Peripheral blood mononuclear cells (PBMC) from NAFLD patients showed higher ROS content and glutathione peroxidase activity and lower glutathione content, superoxide dismutase and glutathione reductase activities than control PBMC. Resistin decreased ROS levels and superoxide dismutase activity and increased glutathione reductase and catalase activities in PBMC from controls but not from patients. Resistin regulates redox homeostasis in mononuclear leukocytes. A decreased response to resistin in leukocytes from NAFLD patients is associated with an impaired redox homeostasis.
Pharmacist and Biochemist, graduated from the University of Buenos Aires, specialist in Hematology and Immunology. Principal professional at the Flow Cytometry and cell Sorting core Facility of the Immunogenetics Laboratory; Institute of Immunology, Genetics and Metabolism (INIGEM), Clinical Hospital José de San Martín, University of Buenos Aires (UBA), National Council for Scientific and Technological Research (CONICET), Buenos Aires, Argentina. Professor of different postgraduate levels courses at the University of Buenos Aires. Member of the River Plate Group of Flow Cytometry. Long experience in Clinical Analysis Diagnosis and Research.
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