Neurosci. 2003 Jul 2;23(13):5816-26.
Novel role of vitamin k in preventing oxidative injury to developing oligodendrocytes and neurons.
Li J, Lin JC, Wang 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.
, 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]Free Article
Note --- there are different kinds of vit K
K1 (phylloquinone) is present naturally in plants.
K2 (menaquinone) is made by bacteria in the intestinal tract of humans and animals
K3 (menadione) is man made.
K4 (menadiol) is man made. It can be used by intestinal bacteria to make K2.
Unlike the fat-soluble compounds K1, K2 and K3, K4 is water-soluble
I know this is last bit of info below is a waste of my time and yours, but here it is...
VINPOCETINE can help remove
Calcium from soft tissues where it does NOT belong.
ViNPOCETINE can help lessen MS activity by up to 48%. Almost ALL Phosphodiesterase inhibitors lower MS activity but the side-effects SUCK. This is not the case for VINPOCETINE.
VINPOCETINE can help with some limited urine flow problems with the bladder.
Taking 30 mg (10 mg 3 times a day) could also make you smart like me.
VINPOCETINE is a Phosphodiesterase inhibitor (TYPE I) PDE1
and causes relaxation of the internal anal sphincter. This loss of sphincter control is a serious problem and really agrivates the constipation problem for many MS folks.
Dis Colon Rectum. 2002 Apr;45(4):530-6.
Phosphodiesterase inhibitors cause relaxation of the internal anal sphincter in vitro.
Jones OM, Brading AF, McC Mortensen NJ.
University Department of Pharmacology, John Radcliffe Hospital, Oxford, United Kingdom.
PURPOSE: Pharmacologic treatments are gaining widespread acceptance as first-line therapy for anal fissure. However, existing treatments have limited clinical usefulness because of side effects and incomplete healing rates.
METHODS: Fresh human surgical resection specimens containing internal anal sphincter and rectal circular muscle were collected. Strips of smooth muscle were cut from each muscle group and mounted in a superfusion organ bath. The effects of increasing concentrations of phosphodiesterase inhibitors were evaluated.
RESULTS: All phosphodiesterase inhibitors tested caused a dose-dependent reduction in the tone of the internal anal sphincter, with potencies as follows: vinpocentine (phosphodiesterase-1 inhibitor; 50 percent maximum inhibition concentration = 0.87 +/- 0.10 microM), erythro-9-(2-hydroxy-3-nonyl) adenine hydrochloride (phosphodiesterase-2 inhibitor; 32 +/- 4.8 microM), trequinsin (phosphodiesterase-3 inhibitor; 0.28 +/- 0.041 microM), rolipram (phosphodiesterase-4 inhibitor; 63 +/- 9 microM), zaprinast (phosphodiesterase-1,5,6,9,11 inhibitor; 3 +/- 0.69 microM), and dipyridamole (phosphodiesterase-5,6,8,10,11 inhibitor; 5.5 +/- 2 microM). Although all inhibitors were also effective on rectal circular muscle strips, erythro-9-(2-hydroxy-3-nonyl) adenine hydrochloride, trequinsin, and rolipram were at least an order of magnitude more potent in this tissue than in the internal anal sphincter.
CONCLUSIONS: There are several functionally important phosphodiesterases in the internal anal sphincter and rectal circular muscle. Both adenosine 3', 5'-cyclic monophosphate and guanosine 3',5'-cyclic monophosphate appear to be important in the myogenic tone of the internal anal sphincter, and this study provides further evidence of the sphincteric specialization of this tissue. Phosphodiesterase inhibitors might represent a new therapy for the treatment of anal fissure.
PMID: 12006938 [PubMed - indexed for MEDLINE]