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There are supposedly two ways a substance is an antioxidant? One being it quenches free radicals
directly or two .. it directly chelates a metal which is causing oxidation. Which of the two would
vitamin K be doing?
J Neurosci. 2003 Jul 2;23(13):5816-26. Related Articles, Links
Novel role of vitamin k in preventing oxidative injury to developing oligodendrocytes and neurons.
Li J, Lin JC, **** H, Peterson JW, Furie BC, Furie B, Booth SL, Volpe JJ, Rosenberg PA.
Department of Neurology, Division of Neuroscience, Children's Hospital, Boston, MA 02115, USA.
Oxidative stress is believed to be the cause of cell death in multiple disorders of the brain,
including perinatal hypoxia/ischemia. Glutamate, cystine deprivation, homocysteic acid, and the
glutathione synthesis inhibitor buthionine sulfoximine all cause oxidative injury to immature
neurons and oligodendrocytes by depleting intracellular glutathione. Although vitamin K is not a
classical antioxidant, we report here the novel finding that vitamin K1 and K2 (menaquinone-4)
potently inhibit glutathione depletion-mediated oxidative cell death in primary cultures of
oligodendrocyte precursors and immature fetal cortical neurons with EC50 values of 30 nm and 2 nm,
respectively. The mechanism by which vitamin K blocks oxidative injury is independent of its only
known biological function as a cofactor for gamma-glutamylcarboxylase, an enzyme responsible for
posttranslational modification of specific proteins. Neither oligodendrocytes nor neurons possess
significant vitamin K-dependent carboxylase or epoxidase activity. Furthermore, the vitamin K
antagonists warfarin and dicoumarol and the direct carboxylase inhibitor 2-chloro-vitamin K1 have
no effect on the protective function of vitamin K against oxidative injury. Vitamin K does not
prevent the depletion of intracellular glutathione caused by cystine deprivation but completely
blocks free radical accumulation and cell death. The protective and potent efficacy of this
naturally occurring vitamin, with no established clinical side effects, suggests a potential
therapeutic application in preventing oxidative damage to undifferentiated oligodendrocytes in
perinatal hypoxic/ischemic brain injury.
PMID: 12843286 [PubMed - indexed for MEDLINE]
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http://pages.ivillage.com/ironjustice/manisaherbivore DEAD PEOPLE WALKING
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directly or two .. it directly chelates a metal which is causing oxidation. Which of the two would
vitamin K be doing?
J Neurosci. 2003 Jul 2;23(13):5816-26. Related Articles, Links
Novel role of vitamin k in preventing oxidative injury to developing oligodendrocytes and neurons.
Li J, Lin JC, **** H, Peterson JW, Furie BC, Furie B, Booth SL, Volpe JJ, Rosenberg PA.
Department of Neurology, Division of Neuroscience, Children's Hospital, Boston, MA 02115, USA.
Oxidative stress is believed to be the cause of cell death in multiple disorders of the brain,
including perinatal hypoxia/ischemia. Glutamate, cystine deprivation, homocysteic acid, and the
glutathione synthesis inhibitor buthionine sulfoximine all cause oxidative injury to immature
neurons and oligodendrocytes by depleting intracellular glutathione. Although vitamin K is not a
classical antioxidant, we report here the novel finding that vitamin K1 and K2 (menaquinone-4)
potently inhibit glutathione depletion-mediated oxidative cell death in primary cultures of
oligodendrocyte precursors and immature fetal cortical neurons with EC50 values of 30 nm and 2 nm,
respectively. The mechanism by which vitamin K blocks oxidative injury is independent of its only
known biological function as a cofactor for gamma-glutamylcarboxylase, an enzyme responsible for
posttranslational modification of specific proteins. Neither oligodendrocytes nor neurons possess
significant vitamin K-dependent carboxylase or epoxidase activity. Furthermore, the vitamin K
antagonists warfarin and dicoumarol and the direct carboxylase inhibitor 2-chloro-vitamin K1 have
no effect on the protective function of vitamin K against oxidative injury. Vitamin K does not
prevent the depletion of intracellular glutathione caused by cystine deprivation but completely
blocks free radical accumulation and cell death. The protective and potent efficacy of this
naturally occurring vitamin, with no established clinical side effects, suggests a potential
therapeutic application in preventing oxidative damage to undifferentiated oligodendrocytes in
perinatal hypoxic/ischemic brain injury.
PMID: 12843286 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------
------
Who loves ya. Tom Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com Man Is A Herbivore!
http://pages.ivillage.com/ironjustice/manisaherbivore DEAD PEOPLE WALKING
http://pages.ivillage.com/ironjustice/deadpeoplewalking