title: Age-related alterations of oxidative stress markers in the mouse hippocampal CA1 sector.
abstract: We investigated the age-related alterations of Cu/Zn-SOD, Mn-SOD, cytochrome c, and HNE (4-hydroxy-2-nonenal) in the hippocampal CA1 sector of 2-, 18-, 40-, 42- and 50-59-week-old mice as compared with 8-week-old mice under the same conditions. Two-week-old mice exhibited small number of Cu/Zn-SOD-positive cells in the hippocampal CA1 sector. Thereafter, Cu/Zn-SOD-positive cells were increased gradually in the hippocampal CA1 sector from 18 to 50-59 weeks of birth. Mn-SOD-positive cells in 2-week-old mice showed a weak staining in the hippocampal CA1 sector. However, Mn-SOD-positive cells were unchanged in the hippocampal CA1 sector from 8 to 50-59 weeks of birth. Cytochrome c-positive cells in 2-week-old mice showed a weak staining in the hippocampal CA1 sector. In contrast, cytochrome c-positive cells were unchanged in the hippocampal CA1 sector up to 40-42 weeks of birth. Thereafter, cytochrome c-positive cells were decreased in the hippocampal CA1 sector of 50-59-week-old mice. HNE immunoreactivity in 2-week-old mice showed a weak density in the hippocampal CA1 sector. In contrast, the density of HNE immunoreactivity was unchanged in the hippocampal CA1 sector up to 40-42 weeks of birth. Thereafter, densities of HNE immunoreactivity were increased significantly in the hippocampal CA1 sector of 50-59-week-old mice. The present results show that the alteration of cytoplasmic Cu/Zn-SOD and lipid peroxidation was more pronounced than that of mitochondrial Mn-SOD in the vulnerable hippocampal CA1 sector during aging processes. Furthermore, the present study demonstrates that the decrease in the number of cytochrome c-positive cells and the increase of densities of HNE immunoreactivity may reflect the mitochondrial dysfunction in the hippocampal CA1 sector of aged animals. These findings suggest that the damage of mitochondrial membrane may occur in the hippocampal CA1 sector during aging processes.
authors.affiliation: Department of Neurobiology and Therapeutics, Graduate School and Faculty of Pharmaceutical Sciences, The University of Tokushima, Tokushima, Japan.
authors.forename: Natsumi
authors.initials: N
authors.lastname: Hayakawa
authors.forename: Hironori
authors.initials: H
authors.lastname: Yokoyama
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kato
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Araki
mesh_terms: D000375:Aging / Q000502:physiology*; D000447:Aldehydes / Q000378:metabolism*; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D045304:Cytochromes c / Q000378:metabolism*; D006624:Hippocampus / Q000166:cytology* / Q000378:metabolism / Q000502:physiology; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D018384:Oxidative Stress / Q000502:physiology*; D013482:Superoxide Dismutase / Q000378:metabolism*
chemical_list: D000447:Aldehydes; D015415:Biomarkers; D045304:Cytochromes c; D013482:Superoxide Dismutase; C027576:4-hydroxy-2-nonenal