Literature DB >> 7564567

Changes in the levels of enzymes which modulate the antioxidant balance occur during aging and correlate with cellular damage.

F Cristiano1, J B de Haan, R C Iannello, I Kola.   

Abstract

Oxidative metabolism produces a flux of superoxide anions that must be removed from the cellular environment if the cell is to survive. The levels of antioxidant enzyme involved in the elimination of superoxide anions and/or hydrogen peroxide were investigated in an attempt to correlate any changes in the levels of these enzymes during aging with changes in free radical mediated cellular damage. Cu/Zn superoxide dismutase (Sod1), glutathione peroxidase (Gpx1) and catalase levels were measured in a number of organs during murine aging. Sod1 enzyme activity rose during aging in all organs studied, while the levels of both Gpx1 and catalase showed organ specific profiles. Both organs in which lipid peroxidation damage (which was used as a marker of free radical mediated damage) increased with age, namely the brain and small intestine, also showed a significant increase in the ratio of Sod1 to Gpx1 enzyme activity. In organs where either the ratio of Sod1/Gpx1 activity or Sod1/catalase levels (in the lung only) ratios were maintained during aging, no increased lipid peroxidation damage was detected. In the lung where Sod1/Gpx1 ratio did increase, Sod1/catalase remained constant and this was able to provide protection during aging. Thus our data shows that alterations in the balance between first and second steps of the antioxidant pathway correlate with cellular damage, and that this may contribute to the aging changes seen in some organs.

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Year:  1995        PMID: 7564567     DOI: 10.1016/0047-6374(94)01561-y

Source DB:  PubMed          Journal:  Mech Ageing Dev        ISSN: 0047-6374            Impact factor:   5.432


  6 in total

1.  Age- and tissue-specific changes in mitochondrial and nuclear DNA base excision repair activity in mice: Susceptibility of skeletal muscles to oxidative injury.

Authors:  Bartosz Szczesny; Anne W Tann; Sankar Mitra
Journal:  Mech Ageing Dev       Date:  2010-04-02       Impact factor: 5.432

2.  Mitochondrial oxidative stress in mice lacking the glutathione peroxidase-1 gene.

Authors:  L A Esposito; J E Kokoszka; K G Waymire; B Cottrell; G R MacGregor; D C Wallace
Journal:  Free Radic Biol Med       Date:  2000-03-01       Impact factor: 7.376

3.  Sensory neurons and schwann cells respond to oxidative stress by increasing antioxidant defense mechanisms.

Authors:  Andrea M Vincent; Koichi Kato; Lisa L McLean; Mary E Soules; Eva L Feldman
Journal:  Antioxid Redox Signal       Date:  2009-03       Impact factor: 8.401

4.  Estimation of the postmortem duration of mouse tissue by electron spin resonance spectroscopy.

Authors:  Shinobu Ito; Tomohisa Mori; Hideko Kanazawa; Toshiko Sawaguchi
Journal:  J Toxicol       Date:  2011-06-27

Review 5.  The Similarities between Human Mitochondria and Bacteria in the Context of Structure, Genome, and Base Excision Repair System.

Authors:  Karolina Boguszewska; Michał Szewczuk; Julia Kaźmierczak-Barańska; Bolesław T Karwowski
Journal:  Molecules       Date:  2020-06-21       Impact factor: 4.411

Review 6.  Oxidative Stress Indexes for Diagnosis of Health or Disease in Humans.

Authors:  Martha A Sánchez-Rodríguez; Víctor Manuel Mendoza-Núñez
Journal:  Oxid Med Cell Longev       Date:  2019-11-25       Impact factor: 6.543

  6 in total

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