title: Changes with age in peritoneal macrophage functions. Implication of leukocytes in the oxidative stress of senescence.
abstract: The age-related deterioration of the immune cells contributes to the increased morbidity and mortality of the aged populations. Since ageing is the result of oxidative stress and macrophages are an important source of oxidation, which is produced in order to carry out many of their functions, the changes with age of several macrophage functions as well as of oxidative stress parameters (oxidants, inflammatory mediators and antioxidants) of peritoneal leukocytes have been investigated using young (4 months), adult (7 months), mature (12 months) and old (20 months) female ICR (CD-1) mice. With age the macrophage functions suffer deterioration. Thus, chemotaxis, phagocytosis and intracellular superoxide anion production decrease in old animals. Moreover, the levels of antioxidant defenses, such as superoxide dismutase activity, decrease with ageing. However, the adherence capacity and the release of oxidant and inflammatory mediators, such as extracellular superoxide anion, TNF-alpha and PGE2, as well as oxidized glutathione/ reduced glutathione ratio, increase with age. These results show that these cells suffer oxidative stress with ageing, which results in an increase of the oxidative damage to nuclear DNA. These changes in peritoneal immune cells could contribute to the chronic oxidative stress state linked to senescence.
authors.affiliation: Department of Animal Physiology, Faculty of Biological Sciences, Complutense University, Madrid 28040, Spain.
authors.forename: M
authors.initials: M
authors.lastname: de la Fuente
authors.forename: A
authors.initials: A
authors.lastname: Hernanz
authors.forename: N
authors.initials: N
authors.lastname: Guayerbas
authors.forename: P
authors.initials: P
authors.lastname: Alvarez
authors.forename: C
authors.initials: C
authors.lastname: Alvarado
mesh_terms: D000818:Animals; D002448:Cell Adhesion / Q000502:physiology; D016922:Cellular Senescence / Q000502:physiology*; D002633:Chemotaxis / Q000502:physiology; D015232:Dinoprostone / Q000032:analysis / Q000378:metabolism; D005260:Female; D005978:Glutathione / Q000032:analysis / Q000378:metabolism; D007962:Leukocytes / Q000502:physiology*; D017737:Macrophages, Peritoneal / Q000378:metabolism / Q000502:physiology*; D051379:Mice; D008813:Mice, Inbred ICR; D018384:Oxidative Stress / Q000502:physiology*; D010587:Phagocytosis / Q000502:physiology; D013482:Superoxide Dismutase / Q000032:analysis / Q000378:metabolism; D013481:Superoxides / Q000032:analysis / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000378:metabolism
chemical_list: D014409:Tumor Necrosis Factor-alpha; D013481:Superoxides; D013482:Superoxide Dismutase; D005978:Glutathione; D015232:Dinoprostone