4.6 Article

Human Plasma Paraoxonase 1 (PON1) Arylesterase Activity During Aging: Correlation with Susceptibility of LDL Oxidation

Journal

ARCHIVES OF MEDICAL RESEARCH
Volume 43, Issue 6, Pages 438-443

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.arcmed.2012.08.012

Keywords

Paraoxonase 1; Low-density lipoproteins; Aging; Plasma; oxidative stress

Funding

  1. Indian Council of Medical Research, New Delhi, India
  2. University Grants Commission Major Research Project Grant [F31-392/2009]

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Background and Aims. The role of free radicals has long been proposed as a cause for the aging process. Oxidative stress is considered a major factor for altering many physiological processes and enzymatic activities during aging and is also known to play a major role in the development of several age-dependent diseases. Paraoxonase 1 (PON1) is an anti-atherosclerotic enzyme that mainly prevents accumulation of lipoperoxides and inhibits the lipid oxidation in low-density lipoproteins (LDL). This study was undertaken to investigate the antioxidant behavior of PON1 by measuring its arylesterase activity. The susceptibility of LDL for oxidation and the radical scavenging activity of plasma were also measured during aging in humans. Methods. Arylesterase activity of PON1 was measured in plasma of human subjects between 20 and 81 years of age of both genders. The susceptibility of LDL for oxidation and radical scavenging activity were measured in plasma. Results. Decrease in plasma arylesterase activity of PON1, increase in susceptibility of LDL for oxidation and decrease in plasma radical scavenging activity were observed as a function of human age. Conclusions. The study provides evidence of a relationship between PON1 activity, LDL oxidation and free radical scavenging activity of plasma. The present results emphasize the dependency of PON1 activity to prevailing oxidative stress during human aging. Our findings assume significance in view of the possible categorization of PON1 as a longevity gene. (C) 2012 IMSS. Published by Elsevier Inc.

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