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The effect of age on protein synthesis in mouse liver

Insights

Protein synthesis declines in old mice due to changes in liver microsomes, not cell sap. This age-related decrease in protein synthesis is linked to reduced messenger RNA content and altered microsomal proteins.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Gerontology

Background:

  • Cellular aging is associated with a decline in protein synthesis.
  • The specific mechanisms underlying age-related decreases in protein synthesis in mammalian liver are not fully understood.

Purpose of the Study:

  • To investigate the age-dependent changes in protein synthesis in mouse liver.
  • To identify whether the decline in protein synthesis is localized to microsomes or the cell-sap fraction.

Main Methods:

  • In vitro protein synthesis assays using liver microsomes and supernatant from young and old mice.
  • Fractionation of microsomes and analysis of ribonucleoprotein particles.
  • Assessment of messenger RNA (mRNA) content and activity.

Main Results:

  • Liver systems from old mice showed reduced incorporation of [(14)C]phenylalanine into protein compared to young mice.
  • The decreased synthetic ability was attributed to changes in microsomes, not the cell-sap fraction.
  • Old mouse microsomes were less responsive to polyuridylic acid (a synthetic mRNA), and senescence correlated with decreased mRNA content.

Conclusions:

  • Aging in mice leads to a decline in liver microsomal protein synthesis.
  • This decline is associated with alterations in microsomal composition, including deletions of detergent-soluble proteins and reduced mRNA content.
  • The findings suggest that decreased mRNA availability and/or function contributes to age-related protein synthesis impairment.

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