Aging and diabetes increase oxidative stress in adipocytes from morbidly obese patients

Resumen del Trabajo presentado al 57º Congreso de La Sociedad Española de Endocrinología y Nutrición, celebrado en Madrid del 27 al 29 de mayo de 2015.-- et al.[Introduction]: Biological systems normally exist in a state of redox homeostasis where antioxidant defenses cope efficiently with the background levels of reactive nitrogen and oxygen species (RNOS). In obese individuals extensive accumulation of fat correlates with oxidative stress in adipose tissue due to the accumulation of RNOS. More specifically, a cellular dysfunction in which mitochondria may play an important role has been pointed out. [Aim]: Proteomic characterization and evaluation of cysteine oxidation in mitochondria isolated from human adipocytes in age-, gender- and phenotype-matched groups of morbidly obese patients by high-throughput proteomic techniques. [Material & Methods]: We purified mitochondria from human adipocytes that were isolated from fresh omental adipose tissue biopsies collected from morbidily obese following bariatric surgery. The oxidation level was assessed in mitochondrial proteins by second generation proteomics strategies based on Filter-Aided Stable Isotope Labeling of Oxidized Cys (FASILOX) and nano high-performance liquid chromatography coupled to mass spectrometry (nHPLC-MS). [Results]: Comparative analyses revealed that both age and diabetes increase global cysteine oxidation levels in mitochondria within the context of obesity. Proteomic results also showed that this oxidation correlates with mitochondrial dysfunction in adipocytes. [Conclusions]: High-throughput proteomic techniques enable reliable detection and quantitation of thousands of proteins in complex proteomes. In this work such proteomic approaches have facilitated the detection of specific cysteine residues differentially oxidized. Future studies on these targets may shed light on the role of oxidative damage in aging and obesity and the development of its related co-morbidities.This work is supported by Grant SAF-2012-33014 (MINECO) (to BP). MG-S is supported by a fellowship from FPI-UAM Program.Peer Reviewe