glucosamine / metal chelator

Discussion in 'Health and medical' started by Doe, Mar 7, 2004.

  1. Doe

    Doe Guest

    These studies seem to tell us the mode of action of
    glucosamine in arthritis is the SAME as the mode of action
    of indocin or indomethacine or .. aspirin .. or .. tagamet
    or .. metal binding.

    <<snip>> Glucosamine is a precursor to a molecule called a
    glycosaminoglycan-this molecule is used in the formation and
    repair of cartilage. Chondroitin is the most abundant
    glycosaminoglycan in cartilage and is responsible for the
    resiliency of cartilage. <<snip>>

    http://tinyurl.com/2be6h

    <<snip>> These outcomes confirm the antioxidant properties
    of GAGs (glycosaminoglycans) and further support the
    hypothesis that these molecules may function as metal
    chelators. <<snip>>

    http://tinyurl.com/25yzo

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  2. Anon

    Anon Guest

    On 2004-03-07 15:57:06 -0500, [email protected] (doe) said:

    > These studies seem to tell us the mode of action of
    > glucosamine in arthritis is the SAME as the mode of action
    > of indocin or indomethacine or .. aspirin .. or .. tagamet
    > or .. metal binding.
    >
    > <<snip>> Glucosamine is a precursor to a molecule called a
    > glycosaminoglycan-this molecule is used in the formation
    > and repair of cartilage. Chondroitin is the most abundant
    > glycosaminoglycan in cartilage and is responsible for the
    > resiliency of cartilage. <<snip>>
    >
    > http://tinyurl.com/2be6h
    >
    > <<snip>> These outcomes confirm the antioxidant properties
    > of GAGs (glycosaminoglycans) and further support the
    > hypothesis that these molecules may function as metal
    > chelators. <<snip>>

    Eh? This is a four-year-old article, basically an opinion
    piece. And where was it published? I didn't think so.
     
  3. Doe

    Doe Guest

    >Subject: Re: glucosamine / metal chelator
    >From: anon [email protected]
    >Date: 3/7/2004 5:11 PM Mountain Standard Time
    >Message-id: <2004030719112650073%[email protected]>
    >
    >On 2004-03-07 15:57:06 -0500, [email protected]
    >(doe) said:
    >
    >> These studies seem to tell us the mode of action of
    >> glucosamine in
    >arthritis is
    >> the SAME as the mode of action of indocin or
    >> indomethacine or .. aspirin ..
    >or
    >> .. tagamet or .. metal binding.
    >>
    >> <<snip>> Glucosamine is a precursor to a molecule called
    >> a glycosaminoglycan-this molecule is used in the
    >> formation and repair of cartilage. Chondroitin is the
    >> most abundant glycosaminoglycan in cartilage and is
    >> responsible for the resiliency of cartilage. <<snip>>
    >>
    >> http://tinyurl.com/2be6h
    >>
    >> <<snip>> These outcomes confirm the antioxidant
    >> properties of GAGs
    >(glycosaminoglycans)
    >> and further support the hypothesis that these molecules
    >> may function as
    >metal
    >> chelators. <<snip>>
    >
    >
    >Eh? This is a four-year-old article, basically an opinion
    >piece. And where was it published? I didn't think so.

    Published in '03 ..

    Glycoconj J. 2003 Feb;20(2):133-41. Links

    Glycosaminoglycans reduce oxidative damage induced by copper
    (Cu(+2)), iron (Fe(+2)) and hydrogen peroxide (H(2)O(2)) in
    human fibroblast cultures.

    Campo GM, D'Ascola A, Avenoso A, Campo S, Ferlazzo AM,
    Micali C, Zanghi L, Calatroni A.

    Department of Biochemical, Physiological and Nutritional
    Sciences, School of Medicine, University of Messina,
    Policlinico Universitario, 98125 Messina, Italy.
    [email protected]

    Acid glycosaminoglycans (GAGs) antioxidant activity was
    assessed in a fibroblast culture system by evaluating
    reduction of oxidative system-induced damage.Three
    different methods to induce oxidative stress in human skin
    fibroblast cultures were used. In the first protocol cells
    were treated with CuSO(4) plus ascorbate. In the second
    experiment fibroblasts were exposed to FeSO(4) plus
    ascorbate. In the third system H(2)O(2) was utilised.The
    exposition of fibroblasts to each one of the three oxidant
    systems caused inhibition of cell growth and cell death,
    increase of lipid peroxidation evaluated by the analysis of
    malondialdehyde (MDA), decrease of reduced glutathione
    (GSH) and superoxide dismutase (SOD) levels, and rise of
    lactate dehydrogenase activity (LDH).The treatment with
    commercial GAGs at different doses showed beneficial
    effects in all oxidative models. Hyaluronic acid (HA) and
    chondroitin-4-sulphate (C4S) exhibited the highest
    protection. However, the cells exposed to CuSO(4) plus
    ascorbate and FeSO(4) plus ascorbate were better protected
    by GAGs compared to those exposed to H(2)O(2).These
    outcomes confirm the antioxidant properties of GAGs and
    further support the hypothesis that these molecules may
    function as metal chelators. Published in 2004.

    PMID: 15001845 [PubMed - in process]

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