Journal
MECHANISMS OF AGEING AND DEVELOPMENT
Volume 126, Issue 10, Pages 1071-1078Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mad.2005.04.001
Keywords
APE1; abasic sited; intracellular distribution; mouse liver
Categories
Funding
- NIA NIH HHS [P01 AG10514] Funding Source: Medline
- NIEHS NIH HHS [R01 ES08457, P01 ES06676] Funding Source: Medline
Ask authors/readers for more resources
The abasic (AP) endonuclease (APE I) plays a central role in the base excision repair (BER) pathway for repairing oxidatively damaged bases and abasic sites in mammalian genomes. We have investigated age-dependent changes in APE activity, contributed primarily by APEI, in total extracts as well as in nuclear, mitochondrial, and cytoplasmic compartments of mouse hepatocytes. The APEI protein and mRNA levels did not differ significantly between the livers of 4-mo (young), 10-mo (middle-aged), and 20-mo (old) mice, and corresponds with similar APE activity. However, we observed a 2-fold increase in specific activity of APEI in the nucleus, a 2-fold decrease in the cytoplasm, and a 6-fold increase in the mitochondrial matrix of hepatocytes of the old relative to the young animals. Surprisingly, in the middle-age animals we observed 30% increase in APE activity in the nucleus but 6-fold in the mitochondrial matrix. These results indicate age-dependent accumulation of APE I in the nucleus and mitochondria. Such redistribution occurred early in the mitochondria during the aging process and preferential accumulation of APE in the nucleus was more gradual which may reflect distinct levels of oxidative stress in these organelles. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available