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Elevated reactive oxygen species and increased mononuclear NADPH oxidase expression in type 2 diabetes patients
Author(s) -
Deo Shekhar H,
Zimmerman Matthew C,
Fadel Paul J
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1137.6
Subject(s) - nadph oxidase , reactive oxygen species , oxidative stress , superoxide , chemistry , superoxide dismutase , medicine , endocrinology , western blot , oxidase test , angiotensin ii , microbiology and biotechnology , receptor , biology , biochemistry , enzyme , gene
Type 2 diabetes (T2D) patients exhibit increased oxidative stress. However, the sources and mechanisms contributing to the elevation in oxidative stress remain unclear. Herein, we sought to examine the potential contribution of the angiotensin II‐NADPH oxidase pathway in mediating the increase in oxidative stress in T2D. In 5 T2D and 5 age‐matched controls, protein expression of NADPH oxidase subunits (gp91 phox , p22 phox , p47 phox and p67 phox ) and angiotensin II type 1 receptor (AT 1 R) were assessed at rest from peripheral blood mononuclear cells using western blot. In addition, electron paramagnetic resonance (EPR) spectroscopy was used to measure blood total reactive oxygen species (ROS) and superoxide. T2D showed elevated resting total ROS (1.3±0.2×10 7 T2D vs. 0.6±0.1×10 7 controls, EPR a.u.; P <0.05) and superoxide (0.3±0.1×10 7 T2D vs. 0.1±0.2×10 7 controls, EPR a.u.; P <0.05) as well as protein expression of all NADPH oxidase subunits ( P <0.05 vs. controls). AT 1 R expression was not different between groups. However, for all subjects, AT 1 R expression was significantly related to all NADPH oxidase subunits (e.g., gp91 phox ; R 2 = 0.53; P <0.05), which in turn was related with total ROS (gp91 phox ; R 2 = 0.59; P <0.05). These preliminary findings suggest that T2D exhibit greater ROS and superoxide that contributes to resting oxidative stress potentially via an up‐regulation of the AT 1 R‐NADPH oxidase pathway.