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1 Department of Neurology, Graduate School of Medicine
2 Laboratory of Aging Study, Graduate School of Human and Environmental Studies, Kyoto University, Japan.
3 Department of Pathology, Institute for Developmental Research, Aichi Human Service Center, Japan.
4 Department of Inflammation Pathology, Faculty of Medicine, Kagawa University, Japan.
5 Graduate School of Science and Technology, Niigata University, Japan.
6 Department of Ultrastructural Research, Institute for Frontier Medical Sciences, Kyoto University, Japan.
Address correspondence to Masanori Hosokawa MD, PhD, Department of Pathology, Institute for Developmental Research, Aichi Human Service Center, 713-8 Kamiya-cho, Kasugai, Aichi 480-0392, Japan. E-mail: hosokawa{at}inst-hsc.jp
The senescence-accelerated mouse is a model for senescence acceleration, a higher oxidative stress status, and age-associated disorders. We studied whether fibroblasts cultured from accelerated senescence-prone SAMP11 mice could be used as in vitro models for oxidative stress in senescence. Dichlorofluorescein and hydroethidine assays demonstrated that cells from SAMP11 mice produced more reactive oxygen species than did cells from accelerated senescence-resistant SAMR1 mice. These differences were not due to the defective induction of antioxidants. Double labeling with hydroethidine and MitoTracker Green revealed that most of the reactive oxygen species were generated within the mitochondria. Nonyl acridine orange and JC-1 assays showed an increase in the mass of the mitochondria, especially those with low membrane potential, in SAMP11 cells. Ultrastructurally, mitochondria with degenerative morphology were increased in SAMP11 cells with longer culture periods. These results suggest that cells from SAMP11 mice are useful models for spontaneous higher oxidative stress in vitro due to dysfunctional mitochondria.
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