metabolic bone diseases / oxidative stress

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  1. Doe

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    Toxicology. 2004 Apr 15;197(2):92-9. Links

    [In Process Citation]

    Isomura H, Fujie K, Shibata K, Inoue N, Iizuka T, Takebe G,
    Takahashi K, Nishihira J, Izumi H, Sakamoto W.

    Department of Biochemistry, School of Dentistry, Hokkaido
    University, North 13 West 7 Kita-ku, Hokkaido, Sapporo
    060, Japan.

    Osteoporosis is associated with many etiological causes such
    as nutrition, cytokines, hormones, and aging. Recently,
    reactive oxygen species (ROS) are considered to be
    responsible for the aging process and osteoporosis. We
    investigated the relationship between ROS and bone
    metabolism in young female and postmenopausal rats, by using
    dietary iron overload and several indices including bone
    metabolic markers, oxidative stress and antioxidant markers,
    and cytokines. Postmenopausal rats exhibited significant
    decreases in serum alkaline phosphatase activity and the
    level of osteocalcin as bone formation markers compared with
    young female rats; however, urinary excretion of
    deoxypyridinoline, a bone resorption marker, did not change.
    On the other hand, a 5% iron lactate diet for 4 weeks in
    postmenopausal rats led to significantly increased excretion
    of urinary deoxypyridinoline and 8-hydroxy-2'-deoxyguanosine
    (8-OHdG) but not serum alkaline phosphatase activity.
    Interestingly, the diet induced significant increases of
    serum osteopontin and TGF-beta1, augumenting osteoclast-
    mediated bone resorption through the RANK/RANKL pathway [J.
    Clin. Invest. 112 (2003) 181]. TGF-beta1 showed a negative
    correlation with serum glutathione peroxidase (GPx) activity
    ( [Formula: see text], [Formula: see text] ), but a positive
    correlation with the serum iron level ( [Formula: see text],
    [Formula: see text] ). Taken together, these results suggest
    for the first time that oxidative stress could be involved
    in the pathogenesis of metabolic bone diseases such as
    osteoporosis as demonstrated by analysis of the relationship
    between bone metabolism and oxidative stress.

    PMID: 15003320 [PubMed - in process]


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