title: Featured Article: Accelerated decline of physical strength in peroxiredoxin-3 knockout mice.
abstract: As a member of peroxiredoxin family, peroxiredoxin-3 plays a major role in the control of mitochondrial level of reactive oxygen species. During the breeding of experimental mice, we noticed that the peroxiredoxin-3 knockout mice were listless with aging. In the present study, we compared the swimming exercise performance and oxidative status between peroxiredoxin-3 knockout mice (n = 15) and wild-type littermates (n = 15). At the age of 10 months, the physical strength of peroxiredoxin-3 knockout mice was much lower than the wild-type littermates. Increased oxidative damage and decreased mitochondrial DNA copy number of the animal skeletal muscles were observed in peroxiredoxin-3 knockout mice as compared to that in the wild-type littermates. In addition, we found increased apoptotic cells in the brains of peroxiredoxin-3 knockout mice. Our results suggest that the deficiency of peroxiredoxin-3 induces accelerated oxidative stress and mitochondrial impairment, resulting in the decrease of energy supply and cellular activities. Peroxiredoxin-3 might be involved in the inhibition of aging process.
authors.affiliation: Department of Obstetrics and Gynecology, Peking University International Hospital, Beijing 102206, China.
authors.forename: Yong-Gang
authors.initials: YG
authors.lastname: Zhang
authors.affiliation: Department of Obstetrics and Gynecology, Yantai Affiliated Hospital of Binzhou Medical University, Yantai 264100, China.
authors.forename: Li
authors.initials: L
authors.lastname: Wang
authors.affiliation: Division of Experimental Animal Immunology, Research Institute for Biomedical Science, Tokyo University of Science, Chiba 278-0022, Japan.
authors.forename: Tomonori
authors.initials: T
authors.lastname: Kaifu
authors.affiliation: School of Basic Medical Sciences, Binzhou Medical University, Yantai 264003, China.
authors.forename: Jingmin
authors.initials: J
authors.lastname: Li
authors.affiliation: School of Basic Medical Sciences, Binzhou Medical University, Yantai 264003, China.
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Obstetrics and Gynecology, Yantai Affiliated Hospital of Binzhou Medical University, Yantai 264100, China lilq2005@bzmc.edu.cn.
authors.forename: Lianqin
authors.initials: L
authors.lastname: Li
mesh_terms: D000375:Aging / Q000378:metabolism / Q000473:pathology / Q000502:physiology; D000818:Animals; D017209:Apoptosis / Q000235:genetics; D015415:Biomarkers / Q000378:metabolism; D056915:DNA Copy Number Variations; D005838:Genotype; D018345:Mice, Knockout; D008928:Mitochondria / Q000378:metabolism; D053580:Muscle Strength / Q000235:genetics*; D018384:Oxidative Stress; D061105:Peroxiredoxin III / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D015415:Biomarkers; D017382:Reactive Oxygen Species; D061105:Peroxiredoxin III
keywords: Peroxiredoxin; aging; mitochondria; oxidative stress; reactive oxygen species