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Aging Liver. A review.

Abhinandana Anantharaju1, Axel Feller, Antonio Chedid

  • 1Department of Medicine, FUHS/Chicago Medical School and Veterans Affairs Medical Center, North Chicago, IL 60064, USA.

Gerontology
|October 24, 2002
PubMed
Summary

Aging affects cellular functions, but the liver maintains relative function. Mitochondrial integrity is preserved, though reactive oxygen species (ROS) damage DNA, and polyunsaturated fatty acids decrease, potentially aiding longevity.

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Area of Science:

  • Gerontology and cellular aging research.
  • Hepatology and metabolic function in aging.
  • Molecular biology of aging and senescence.

Background:

  • Aging is a progressive decline in cellular functions, with the liver showing relative functional preservation.
  • Morphological changes in the aging liver include decreased size due to reduced hepatic blood flow.
  • Mitochondrial integrity and enzymatic activity in the human liver remain largely unchanged with age.

Purpose of the Study:

  • To explore the multifaceted impact of aging on liver function and cellular processes.
  • To investigate the role of reactive oxygen species (ROS) and DNA damage in liver aging.
  • To examine the influence of diet, drug metabolism, and telomere dynamics on lifespan and cellular senescence.

Main Methods:

  • Ultrastructural analysis of human liver tissue to assess mitochondrial integrity.
  • Examination of reactive oxygen species (ROS) generation and its impact on mitochondrial DNA.
  • Analysis of polyunsaturated fatty acid levels in liver mitochondria of centenarians.
  • Investigation of the ubiquitin-proteolytic pathway and p21 expression in senescent cells.
  • Review of factors affecting drug metabolism (cytochrome P450) and therapy in the elderly.
  • Exploration of telomere shortening and telomerase activity in relation to cellular replicative lifespan.

Main Results:

  • While liver function is relatively preserved, aging is associated with decreased liver size and hepatic blood flow.
  • Reactive oxygen species (ROS) contribute to mitochondrial DNA damage, which accumulates with aging.
  • Polyunsaturated fatty acids decrease in liver mitochondria of centenarians, a potential longevity mechanism.
  • The ubiquitin-proteolytic pathway, including p21, plays a role in managing senescent cells and DNA repair.
  • Hepatic drug metabolism via cytochrome P450 declines with age, increasing adverse drug reaction risk in the elderly.
  • Telomere shortening correlates with cellular replicative senescence, while telomerase activity can extend lifespan.

Conclusions:

  • The aging liver exhibits specific adaptations, including reduced ROS-sensitive fatty acids, potentially for longevity.
  • Cellular senescence, regulated by pathways like ubiquitin-proteolysis and telomere dynamics, acts as a protective mechanism against uncontrolled cell division and mutation.
  • Understanding age-related changes in liver function, drug metabolism, and cellular senescence is crucial for geriatric care and longevity research.

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