vitamin-k-semiquinone-radical and Nerve-Degeneration

Vitamin K has several biological effects and dietary intake seems to be more important than previously believed because of low bioavailability of the vitamins from the colon.. Data from the literature were identified on PubMed, and data from NORKOST II (a dietary study from 1997 based on a nation-wide sample of respondents) were used to calculate dietary intake of vitamin K.. The dietary intake of vitamin K in Norway seems to be < 50% of what is recommended. The stores of vitamin K are small and T/2 in the body is approximately 1-1.5 day. Vitamin K executes its effects by carboxylation of proteins and as ligand (vitamin K2) for a nuclear transcription factor. Biological effects beyond coagulation include bone formation, neural functioning and blood vessel calcification. Anticoagulation with warfarin inhibits vitamin K-dependent reactions and may have detrimental effects on bone formation.. It is possible that the high incidence of osteoporosis in Norway may be due to the low dietary intake of vitamin K, hence it is suggested that the intake of vitamin K should be increased and vitamin K antagonists be replaced with specific thrombin inhibitors. New technology allows measurements of plasma concentration of vitamin K in relation to malabsorption, insufficient diet, and osteoporosis.

Topics: Adult; Blood Coagulation; Bone Density; Calcinosis; Child; Female; Food Analysis; Humans; Male; Nerve Degeneration; Norway; Nutritional Requirements; Osteoporosis; Vitamin K

Vitamin K (VK) has a protective effect on neural cells. Methylmercury is a neurotoxicant that directly induces neuronal death in vivo and in vitro. Therefore, in the present study, we hypothesized that VK inhibits the neurotoxicity of methylmercury. To prove our hypothesis in vitro, we investigated the protective effects of VKs (phylloquinone, vitamin K(1); menaquinone-4, vitamin K(2) ) on methylmercury-induced death in primary cultured neurons from the cerebella of rat pups. As expected, VKs inhibited the death of the primary cultured neurons. It has been reported that the mechanisms underlying methylmercury toxicity involve a decrement of intracellular glutathione (GSH). Actually, treatment with GSH and a GSH inducer, N-acetyl cysteine, inhibited methylmercury-induced neuronal death in the present study. Thus, we investigated whether VKs also have protective effects against GSH-depletion-induced cell death by employing two GSH reducers, L-buthionine sulfoximine (BSO) and diethyl maleate (DEM), in primary cultured neurons and human neuroblastoma IMR-32 cells. Treatment with VKs affected BSO- and DEM-induced cell death in both cultures. On the other hand, the intracellular GSH assay showed that VK(2), menaquinone-4, did not restore the reduced GSH amount induced by methylmercury or BSO treatments. These results indicate that VKs have the potential to protect neurons against the cytotoxicity of methylmercury and agents that deplete GSH, without increasing intracellular GSH levels. The protective effect of VKs may lead to the development of treatments for neural diseases involving GSH depletion.

Topics: Animals; Animals, Newborn; Cell Death; Cell Line, Tumor; Disease Models, Animal; Humans; In Vitro Techniques; Mercury Poisoning, Nervous System; Methylmercury Compounds; Nerve Degeneration; Neurons; Neuroprotective Agents; Rats; Rats, Wistar; Vitamin K