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Systemic oxidative stress in older adults: Do peripheral blood mononuclear cells contribute?
Author(s) -
Schanzle Jennifer C,
Deo Shekhar H,
Fadel Paul J
Publication year - 2013
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.27.1_supplement.1142.6
Subject(s) - sod2 , oxidative stress , nadph oxidase , peripheral blood mononuclear cell , superoxide dismutase , sod1 , superoxide , reactive oxygen species , medicine , endocrinology , immunology , intracellular , chemistry , enzyme , biochemistry , in vitro
Although it is well known that systemic oxidative stress increases with age, the sources and mechanisms contributing to aging induced increase in oxidative stress remain unclear. Recent findings in animals indicate that peripheral blood mononuclear cells (PBMCs) are a major source of systemic oxidative stress via stimulation of the angiotensin II type 1 receptor (AT 1 R)‐NADPH oxidase pathway. Thus, to better understand this pathway and its potential contribution to increased oxidative stress with age, PBMCs were isolated from whole blood in healthy recreationally active older (61 ± 2 years, n=5) and younger men (25 ± 2 years, n=7). Intracellular superoxide production was measured using dihydroethidium fluorescence and NADPH oxidase subunits (gp91 phox , p22 phox , and p67 phox ) and superoxide dismutase 1 and 2 (SOD1 and SOD2) mRNA expression was measured using real time RT‐PCR. Interestingly, intracellular superoxide production was similar between groups (2 ± 0.4 older vs. 2 ± 0.3 young, Relative Fluorescence Units; P >;0.05). Likewise, gp91 phox and p22 phox were not different between groups, whereas p67 phox was actually significantly lower in older subjects. Aging did not influence SOD2 mRNA expression, while SOD1 expression was lower in older subjects. These preliminary findings suggest that PBMCs may not be a primary source of systemic oxidative stress in healthy older individuals. Supported by NIH Grant R01 HL093167