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DNA double-strand breaks in mouse kidney cells with age

N P Singh1, C E Ogburn, N S Wolf

  • 1Department of Bioengineering, University of Washington, Seattle 98195, USA. narendra@u.washington.edu

Biogerontology
|March 1, 2002
PubMed

Insights

Aging increases DNA double-strand breaks in mouse kidney cells, correlating with greater kidney pathology. This age-related DNA damage is modest but significant, highlighting cellular changes during the aging process.

Area of Science:

  • Gerontology
  • Molecular Biology
  • Genetics

Background:

  • Cellular aging is associated with accumulating DNA damage.
  • Understanding age-related DNA damage in specific organs like the kidney is crucial for aging research.

Purpose of the Study:

  • To quantify DNA double-strand breaks (DSBs) in kidney cells of middle-aged and old mice.
  • To investigate the correlation between DNA damage and kidney pathology in aging.

Main Methods:

  • Single cell suspensions were prepared from C57B1/6 mouse kidneys (12- and 24-month-old) using a Biojector device.
  • Microgel electrophoresis was employed to detect and quantify DNA double-strand breaks.
  • DNA damage levels were compared to a calibration curve using X-ray-induced damage.

Main Results:

  • A significant 7.3% increase in DNA double-strand breaks was observed in kidney cells of old (24-month-old) mice compared to middle-aged (12-month-old) mice (P = 0.04).
  • The observed increase in DNA damage is equivalent to that induced by 0.1 Gray of X-rays.
  • Higher levels of DNA damage positively correlated with increased kidney pathology in older mice.

Conclusions:

  • Kidney cells accumulate DNA double-strand breaks with age in C57B1/6 mice.
  • Age-related DNA damage in the kidney is linked to the development of organ pathology.
  • These findings contribute to understanding the molecular mechanisms of aging and organ decline.

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