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Oxidative status in senescence-accelerated mice

J W Park1, C H Choi, M S Kim

  • 1Department of Pharmacology, Seoul National University College of Medicine, Chongno-gu, Korea.

The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
|September 1, 1996
PubMed
Summary
This summary is machine-generated.

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Accelerated senescence in mice is linked to reduced antioxidant defenses. Impaired transport of copper-zinc superoxide dismutase (Cu,Zn-SOD) into mitochondria contributes to oxidative stress and faster aging.

Area of Science:

  • Gerontology
  • Biochemistry
  • Cell Biology

Background:

  • Senescence-accelerated mice (SAM) models exhibit varying aging rates.
  • Oxidative stress and lipid peroxidation are implicated in aging processes.
  • Antioxidant enzymes play a crucial role in cellular defense against damage.

Purpose of the Study:

  • To investigate lipid peroxidation and antioxidant enzyme activities in senescence-resistant (SAM-R/1) and senescence-prone (SAM-P/1) mice.
  • To identify molecular mechanisms underlying accelerated aging in SAM-P/1 mice.
  • To assess the role of mitochondrial superoxide dismutase (SOD) in senescence.

Main Methods:

  • Comparative analysis of liver tissues from SAM-R/1 and SAM-P/1 substrains across different ages.
  • Quantification of lipid peroxidation products (fluorescent age pigment, conjugated dienes).

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  • Measurement of antioxidant enzyme activities, focusing on mitochondrial Cu,Zn-SOD, and assessment of its mRNA levels.

    • Main Results:

    • Higher levels of lipid peroxidation products were observed in SAM-P/1 mice compared to SAM-R/1 mice, increasing with age.
    • Mitochondrial superoxide dismutase (SOD) activity was significantly decreased in SAM-P/1 mice across all age groups.
    • Reduced mitochondrial Cu,Zn-SOD protein levels were found in SAM-P/1 mice, despite comparable mRNA levels to SAM-R/1 mice.

    Conclusions:

    • Impaired mitochondrial import of Cu,Zn-SOD, rather than reduced synthesis, is a key factor in decreased antioxidant defense in SAM-P/1 mice.
    • This reduction in defense against oxidative stress likely contributes to the accelerated senescence phenotype observed in SAM-P/1 mice.
    • Targeting mitochondrial protein transport may offer therapeutic strategies for age-related decline.