Mood stabilizers / oxidative damage / lithium and valproate

Discussion in 'Food and nutrition' started by [email protected], Jan 5, 2006.

  1. Chronic treatment with mood stabilizers lithium and valproate prevents
    excitotoxicity by inhibiting oxidative stress in rat cerebral cortical
    cells.
    Shao L, Young LT, Wang JF
    Biol Psychiatry. 2005 Dec 1; 58(11): 879-84

    BACKGROUND:
    Recent studies indicate that chronic treatment with the
    mood-stabilizing drugs lithium and valproate produces a neuroprotective
    effect against excitotoxicity.
    In this study, we aimed to determine whether inhibiting oxidative
    damage plays a role in a neuroprotective effect of lithium and
    valproate against excitotoxicity.
    METHODS:
    Intracellular free calcium concentration was measured with the
    fluorescent calcium ion indicator fluo-3. Malondialdehyde, an end
    product derived from peroxidation of polyunsaturated fatty acid, and
    protein carbonyls were used to assess oxidative damage to lipid and
    protein. Excitotoxicity was assayed by measuring cell viability with
    the MTT [3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl tetrazolium bromide]
    method and by measuring deoxyribonucleic acid (DNA) fragmentation with
    TUNEL (terminal deoxynucleotidyltransferase-mediated deoxyuridine
    triphosphate nick end labeling) staining. RESULTS:
    We found that chronic treatment with lithium and valproate at their
    therapeutically relevant concentrations significantly inhibited the
    glutamate-induced increase of intracellular free calcium concentration,
    lipid peroxidation, protein oxidation, DNA fragmentation, and cell
    death in primary cultured rat cerebral cortical cells.
    This treatment had no effect on basal intracellular free calcium
    concentration, lipid peroxidation, protein oxidation, DNA
    fragmentation, and cell death.
    CONCLUSIONS: Our results suggest that chronic treatment with lithium
    and valproate inhibits oxidative damage to lipid and protein and in
    turn produces a neuroprotective effect against excitotoxicity.


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