X-Message-Number: 25536
Date: Thu, 13 Jan 2005 18:26:26 -0800 (PST)
From: Doug Skrecky <>
Subject: vitamin K2 as a life extender?

["Vitamin K .... completely blocks free radical accumulation and cell death"]

J Neurosci. 2003 Jul 2;23(13):5816-26
Novel role of vitamin k in preventing oxidative injury to developing
oligodendrocytes and neurons.
  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.

J Nutr. 2004 Nov;134(11):3100-5.
Dietary intake of menaquinone is associated with a reduced risk of
coronary heart disease: the Rotterdam Study.
  Vitamin K-dependent proteins, including matrix Gla-protein, have been
shown to inhibit vascular calcification. Activation of these proteins via
carboxylation depends on the availability of vitamin K. We examined
whether dietary intake of phylloquinone (vitamin K-1) and menaquinone
(vitamin K-2) were related to aortic calcification and coronary heart
disease (CHD) in the population-based Rotterdam Study. The analysis
included 4807 subjects with dietary data and no history of myocardial
infarction at baseline (1990-1993) who were followed until January 1,
2000. The risk of incident CHD, all-cause mortality, and aortic
atherosclerosis was studied in tertiles of energy-adjusted vitamin K
intake after adjustment for age, gender, BMI, smoking, diabetes,
education, and dietary factors. The relative risk (RR) of CHD mortality
was reduced in the mid and upper tertiles of dietary menaquinone
compared to the lower tertile [RR = 0.73 (95% CI: 0.45, 1.17) and 0.43
(0.24, 0.77), respectively]. Intake of menaquinone was also inversely
related to all-cause mortality [RR = 0.91 (0.75, 1.09) and 0.74 (0.59,
0.92), respectively] and severe aortic calcification [odds ratio of 0.71
(0.50, 1.00) and 0.48 (0.32, 0.71), respectively]. Phylloquinone intake
was not related to any of the outcomes. These findings suggest that an
adequate intake of menaquinone could be important for CHD prevention.

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