This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Naiki, H. Articles by Takeda, T. Search for Related Content PubMed PubMed Citation Articles by Naiki, H. Articles by Takeda, T.

American Journal of Pathology, Vol 130, 579-587, Copyright © 1988 by American Society for Investigative Pathology

REGULAR ARTICLES

Metabolism of senile amyloid precursor and amyloidogenesis. Age-related acceleration of apolipoprotein A-II clearance in the senescence accelerated mouse

H Naiki, K Higuchi, T Yonezu, M Hosokawa and T Takeda
Department of Pathology, Kyoto University, Japan.

Serum clearance kinetics of murine senile amyloid-related high-density lipoprotein (HDL) apoprotein A-II (apo A-II) was examined in the senescence-accelerated mouse, prone (SAM-P/1) and resistant (SAM-R/1), with 125I-HDL purified from both strains. In SAM-R/1, with 125I-HDL purified from both strains. In SAM-R/1, the serum half-life of apo A-II was not altered with increasing age and was practically identical to that of apo A-I. In 2-month old SAM-P/1, the serum half-life of both apo A-I and apo A-II was generally the same as observed in SAM-R/1. However, at age 6 and 12 months, in SAM-P/1, the serum half-life of apo A-II decreased significantly and was less than that of apo A-I. These age-related changes in apo A-II clearance kinetics were observed regardless of the HDL donor. The authors also examined the tissue distribution of injected apo A-II, using 125I-apo A-II reconstituted HDL, and found that several organs trapped more 125I radioactivity in old SAM-P/1 than in young mice. This evidence strongly suggests that age-related changes in the metabolic environment of apo A-II might affect senile amyloidogenesis in SAM-P/1.

This article has been cited by other articles:

				W. Jin, G.-S. Sun, D. Marchadier, E. Octtaviani, J. M. Glick, and D. J. Rader Endothelial Cells Secrete Triglyceride Lipase and Phospholipase Activities in Response to Cytokines as a Result of Endothelial Lipase Circ. Res., April 4, 2003; 92(6): 644 - 650. [Abstract] [Full Text] [PDF]

				M. Umezawa, K. Tatematsu, T. Korenaga, X. Fu, T. Matushita, H. Okuyama, M. Hosokawa, T. Takeda, and K. Higuchi Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the senescence- accelerated mouse J. Lipid Res., April 1, 2003; 44(4): 762 - 769. [Abstract] [Full Text] [PDF]

				L. Fu, I. Matsuyama, T. Chiba, Y. Xing, T. Korenaga, Z. Guo, X. Fu, J. Nakayama, M. Mori, and K. Higuchi Extrahepatic Expression of Apolipoprotein A-II in Mouse Tissues: Possible Contribution to Mouse Senile Amyloidosis J. Histochem. Cytochem., June 1, 2001; 49(6): 739 - 748. [Abstract] [Full Text]

				J. Wang, T. Matsushita, K. Kogishi, C. Xia, A. Ohta, T. Chiba, A. Nakamura, H. Kondo, M. Mori, M. Hosokawa, et al. Wild Type ApoA-II Gene Does Not Rescue Senescence-Accelerated Mouse (SAMP1) From Short Life Span and Accelerated Mortality J. Gerontol. A Biol. Sci. Med. Sci., September 1, 2000; 55(9): 432B - 439. [Abstract] [Full Text]