An aging-related cell surface NADH oxidase (arNOX) generates superoxide and is inhibited by coenzyme Q

This report describes a novel ECTO-NOX protein with an oscillating activity having a period length of ca. 26 min encountered with buffy coat fractions and sera of aged individuals (70-100 years) that generates superoxide as measured by the reduction of ferricytochrome c. The oscillating, age-related...

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Bibliographic Details
Published in:Molecular and cellular biochemistry 2003-12, Vol.254 (1-2), p.101-109
Main Authors: Morré, Dorothy M, Guo, Fenghui, Morré, D James
Format: Article
Language:English
Subjects:
Adult
Age Factors
Aged
Aged, 80 and over
Aging
Cell Membrane - enzymology
Cytochrome Reductases - chemistry
Cytochromes c - chemistry
Endopeptidase K - chemistry
Enzymatic activity
Enzymes
Humans
Kinetics
Middle Aged
Multienzyme Complexes - chemistry
Multienzyme Complexes - physiology
NADH, NADPH Oxidoreductases - chemistry
NADH, NADPH Oxidoreductases - physiology
Oscillometry
Oxidative Stress
Oxygen - metabolism
Superoxide Dismutase - chemistry
Superoxides - chemistry
Time Factors
Ubiquinone - pharmacology
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Summary:This report describes a novel ECTO-NOX protein with an oscillating activity having a period length of ca. 26 min encountered with buffy coat fractions and sera of aged individuals (70-100 years) that generates superoxide as measured by the reduction of ferricytochrome c. The oscillating, age-related reduction of ferricytochrome c is sensitive to superoxide dismutase, is inhibited by coenzyme Q and is reduced or absent from sera of younger individuals (20-40 years). An oscillating activity with a regular period length is a defining characteristic of ECTO-NOX proteins (a group of cell surface oxidases with enzymatic activities that oscillate). The period length of ca. 26 min is longer than the period length of 24 min for the usual constitutive (CNOX) ECTO-NOX proteins of the cell surface and sera which neither generate superoxide nor reduce ferricytochrome c. The aging-related ECTO-NOX protein (arNOX) provides a mechanism to transmit cell surface oxidative changes to surrounding cells and circulating lipoproteins potentially important to atherogenesis. Additionally, the findings provide a rational basis for the use of dietary coenzyme Q to retard aging-related arterial lesions.
ISSN:0300-8177
1573-4919
DOI:10.1023/A:1027301405614