Recent evidence from
apolipoprotein E-deficient (
apoE-/-) mice shows that aging and
atherosclerosis are closely associated with increased oxidative stress and DNA damage in some cells and tissues. However, bone marrow cells, which are physiologically involved in tissue repair have not yet been investigated. In the present study, we evaluated the influence of aging and
hypercholesterolemia on oxidative stress, DNA damage and apoptosis in bone marrow cells from young and aged
apoE-/- mice compared with age-matched wild-type C57BL/6 (C57) mice, using the comet assay and flow cytometry. The production of both
superoxide and
hydrogen peroxide in bone marrow cells was higher in young
apoE-/- mice than in age-matched C57 mice, and
reactive oxygen species were increased in aged C57 and
apoE-/- mice. Similar results were observed when we analyzed the DNA damage and apoptosis. Our data showed that both aging and
hypercholesterolemia induce the increased production of oxidative stress and consequently DNA damage and apoptosis in bone marrow cells. This study is the first to demonstrate a functionality decrease of the bone marrow, which is a fundamental extra-arterial source of the cells involved in
vascular injury repair.