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Quercetin treatment reverses cognitive deficits

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General fitness, health and nutrition
Published
6 January 2004
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14 January 2004
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Doe
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  1. Free Radic Res. 2003 Nov;37(11):1245-52. Links

    Reversal of aging and chronic ethanol-induced cognitive dysfunction by quercetin a bioflavonoid.

    Singh A, Naidu PS, Kulkarni SK.

    Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh-
    160014, India.

    Cognitive dysfunction, one of the most striking age-related impairments seen in human beings, has
    been correlated to the vulnerability of the brain to increased oxidative stress during aging
    process. Quercetin is a bioflavonoid with strong antioxidant properties. Experiments were performed
    to study the possible effects of quercetin on cognitive performance of young, aged or ethanol-
    intoxicated mice (an animal model for cognition dysfunction) using one trail step down type of
    passive avoidance and elevated plus maze tasks, respectively. Aged or chronic ethanol-treated mice
    showed poor retention of memory in step-down passive avoidance and in elevated plus-maze task.
    Chronic administration of quercetin (10, 25 and 50 mg/kg) for 30 days or its co-administration with
    ethanol (15% w/v, 2g/kg per orally) for 24 days significantly reversed the age-related or chronic
    ethanol-induced retention deficits in both the test paradigms. However, in both memory paradigms
    chronic administration of quercetin failed to modulate the retention performance of young mice.
    Chronic quercetin administration for 30 days also reversed age associated increase in TBARS levels
    and decline in forebrain total glutathione (GSH), SOD and catalase levels. Chronic ethanol
    administration to young mice produced an increase in lipid peroxidation, and a decline in forebrain
    total glutathione (GSH), SOD and catalase levels, which was significantly reversed by the co-
    administration of quercetin (10, 25 and 50 mg/kg). The results of the present study showed that
    chronic quercetin treatment reverses cognitive deficits in aged and ethanol-intoxicated mice, which
    is associated with its antioxidant property.

    PMID: 14703737 [PubMed - in process]

    --------------------------------------------------------------------------
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  2. Quoted message said:

    Subject: Quercetin treatment reverses cognitive deficits

    Free Radic Biol Med. 2002 Jul 1;33(1):63-70. elsevier.nlindex.htt

    Protection against oxidative damage of erythrocyte membrane by the flavonoid quercetin and its
    relation to iron chelating activity

    --------------------------------------------------------------------------
    ------------------------------------
    Quercetin metabolism in the lens: role in inhibition of hydrogen peroxide induced cataract.

    Cornish KM, Williamson G, Sanderson J.

    School of Biological Sciences, University of East Anglia, Norwich, Norfolk, UK.

    Oxidative stress is implicated in the initiation of maturity onset cataract. Quercetin, a major
    flavonol in the diet, inhibits lens opacification in a lens organ culture oxidative model of
    cataract. The aim of this research was to investigate the metabolism of quercetin in the lens and
    show how its metabolism affects the ability to prevent oxidation-induced opacity. The LOCH model
    (Free Radical Biology & Medicine 26:639; 1999) was employed, using rat lenses to investigate the
    effects of quercetin and metabolites on hydrogen peroxide-induced opacification. High-performance
    liquid chromatography analysis showed that the intact rat lens is capable of converting quercetin
    aglycone to 3'-O-methyl quercetin (isorhamnetin). Over a 6 h culture period no further metabolism of
    the 3'-O-methyl quercetin occurred. Loss of quercetin in the lens was accounted for by the increase
    in 3'-O-methyl quercetin. Incubation with 3,5-dinitrocatechol (10 microM), a catechol-O-
    methyltransferase (COMT) inhibitor, prevented the conversion of quercetin to 3'-O- methyl quercetin.
    The presence of both membrane-bound and soluble COMT was confirmed by immunoblotting. The results
    demonstrate that in the rat lens COMT methylates quercetin and that the product accumulates within
    the lens. Quercetin (10 microM) and 3'-O-methyl quercetin (10 microM) both inhibited hydrogen peroxide-
    (500 microM) induced sodium and calcium influx and lens opacification. Incubation of lenses with
    quercetin in the presence of COMT inhibitor revealed that the efficacy of quercetin is not dependent
    on its metabolism to 3'-O-methyl quercetin. The results indicate dietary quercetin and metabolites
    are active in inhibiting oxidative damage in the lens and thus could play a role in prevention of
    cataract formation.

    PMID: 12086683 [PubMed - indexed for MEDLINE

    Who loves ya. Tom

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  3. I thought it inhibited the formation of cataracts by inhibiting aldol reductase and thereby reducing
    sorbitol levels in the lens.

    "doe" <[email hidden]> wrote in message "]news:[email hidden]...

    Quoted message said:
    Quoted message said:

    Subject: Quercetin treatment reverses cognitive deficits

    Free Radic Biol Med. 2002 Jul 1;33(1):63-70. elsevier.nlindex.htt

    Protection against oxidative damage of erythrocyte membrane by the


    flavonoid

    Quoted message said:

    quercetin and its relation to iron chelating activity

    --------------------------------------------------------------------------
    ------------------------------------
    Quercetin metabolism in the lens: role in inhibition of hydrogen peroxide induced cataract.

    Cornish KM, Williamson G, Sanderson J.

    School of Biological Sciences, University of East Anglia, Norwich, Norfolk, UK.

    Oxidative stress is implicated in the initiation of maturity onset cataract. Quercetin, a major
    flavonol in the diet, inhibits lens opacification in a lens organ culture oxidative model of
    cataract. The aim of this research was to investigate the metabolism of quercetin in the lens and
    show how its metabolism affects the ability to prevent oxidation-induced opacity. The LOCH model
    (Free Radical Biology & Medicine 26:639; 1999) was employed, using rat lenses to investigate the
    effects of quercetin and metabolites on hydrogen peroxide-induced opacification. High-performance
    liquid chromatography analysis showed that the intact rat lens is capable of converting quercetin
    aglycone to 3'-O-methyl quercetin (isorhamnetin). Over a 6 h culture period no further metabolism
    of the 3'-O-methyl quercetin occurred. Loss of quercetin in the lens was accounted for by the
    increase in 3'-O-methyl quercetin. Incubation with 3,5-dinitrocatechol (10 microM), a catechol-O-
    methyltransferase (COMT) inhibitor, prevented the conversion of quercetin to 3'-O- methyl
    quercetin. The presence of both membrane-bound and soluble COMT was confirmed by immunoblotting.
    The results demonstrate that in the rat lens COMT methylates quercetin and that the product
    accumulates within the lens. Quercetin (10 microM) and 3'-O-methyl quercetin (10 microM) both
    inhibited hydrogen peroxide- (500 microM) induced sodium and calcium influx and lens
    opacification. Incubation of lenses with quercetin in the presence of COMT inhibitor revealed that
    the efficacy of quercetin is not dependent on its metabolism to 3'-O-methyl quercetin. The results
    indicate dietary quercetin and metabolites are active in inhibiting oxidative damage in the lens
    and thus could play a role in prevention of cataract formation.

    PMID: 12086683 [PubMed - indexed for MEDLINE

    Who loves ya. Tom

    Jesus Was A Vegetarian! jesuswasavegetarian.7h.comjesuswasavegetarian.7h.com Man Is A Herbivore!
    pages.ivillage.commanisaherbivore DEAD PEOPLE WALKING


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