Mitochondrial dysfunction in platelets and hippocampi of senescence-accelerated mice.
Senescence-accelerated mice (SAM) strains are useful models to understand the mechanisms of age-dependent degeneration. In this study, measurements of the mitochondrial membrane potential (Deltapsi(m)) of platelets and the Adenosine 5(')-triphosphate (ATP) content of hippocampi and platelets were made, and platelet mitochondria were observed in SAMP8 (faster aging mice) and SAMR1 (aging resistant control mice) at 2, 6 and 9 months of age. In addition, an Abeta-induced (Amyloid beta-protein) damage model of platelets was established. After the addition of Abeta, the Deltapsi(m) of platelets of SAMP8 at 1 and 6 months of age were measured. We found that platelet Deltapsi(m), and hippocampal and platelet ATP content of SAMP8 mice decreased at a relatively early age compared with SAMR1. The platelets of 6 month-old SAMP8 showed a tolerance to Abeta-induced damages. These results suggest that mitochondrial dysfunction might be one of the mechanisms leading to age-associated degeneration in SAMP mice at an early age and the platelets could serve as a biomarker for detection of mitochondrial function and age related disease.
Xu
Jie
J
Department of Anatomy, Zhongshan School of Medicine, Sun Yat-Sen University Guangzhou, Guangdong 510080, China.
Shi
Chun
C
Li
Qi
Q
Wu
Jiajia
J
Forster
E Lucy
EL
Yew
David T
DT
D000255:Adenosine Triphosphate / Q000378:metabolism; D000375:Aging / Q000502:physiology*; D016229:Amyloid beta-Peptides / Q000494:pharmacology; D000818:Animals; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D006624:Hippocampus / Q000502:physiology* / Q000648:ultrastructure; D053078:Membrane Potential, Mitochondrial; D051379:Mice; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology*; D010446:Peptide Fragments / Q000494:pharmacology
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42); D000255:Adenosine Triphosphate