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Introduction: Vitamin K is well known for its role in the synthesis of many blood coagulation factors. Also, vitamin K-dependent proteins are very important for bone and vascular health. Vitamin K is known to influence bone metabolism by facilitating the synthesis of osteocalcin because is required for the γ-carboxylation of specific glutamic acid residues, wich in turn, allows a firm binding of calcium ions. The bone mineral density decreases drastically after menopause. Recent studies have been shown that vitamin k influences bone mineral density in osteoporotic people and also actually reduce fracture rates. Many factors influence the individual risk of osteoporosis: genetic predisposition, age, sex, race, general health, exercise, smoking, alcohol abuse, hormone therapy and nutritional factors. In fact, current research is emphasizing the role of nutrition in the development of this disease and has been focused on calcium, magnesium, vitamin D roles and macronutrients such as proteins. In the present study, we investigated the relationship between vitamin K1 and K2 levels and bone mineral density in post-menopausal women. Materials and methods: Serum levels of vitamins K1 and K2, osteocalcin and other markers of bone metabolism were measured in 100 post-menopausal women (19 with reduced bone mineral density and 52 with normal bone density). Vitamin K1 and K2 levels were measured by HPLC method. The vitamins in plasma were analyzed by reversed-HPLC with UV detection at 250 nm. The mobile phase was methanol and ethanol (85:15,v/v) with 0.1 % triethylamine. Results: The mean concentration (± SE)of vitamin K1 in the normal bone density group was 0.60±0.03 ng/ml, in the reduced bone density group was 0.36±0.02 ng/ml. The mean concentration (± SE)of vitamin K2 in the normal one was 1.0±0.04 ng/ml, in the reduced one was 0.72±0.02 ng/ml. Post-menopausal women with reduced bone mineral density showed lower levels of vitamins K1 and K2 than those with normal bone mineral density. Conclusions: The present findings suggested that vitamin K level is related to post-menopausal bone mineral loss. An extension of this theory is that Vitamin B6 is an essential cofactor for the ornithine decarboxylase, which regulates osteoblast glucose-6-phosphate dehydrogenase activity and thus NADPH concentrations: this is essential for the vitamin K cycle, where its epoxide form is converted to the naphtoquinone form, required for γ-carboxylation of osteocalcin. Thus, probably, the vitamin B6 status could modulate the effects of vitamin K on bone metabolism. References:Vermeer C., et al. (2004) Eur J nutr 43: 325-335. 260 biochimica

A major unanswered question is whether direct cellular toxicity of homocysteine (Hcy) is causally involved in cardiovascular disease (CVD) in humans or whether homocysteinemia is simply a passive and indirect indicator of a more complex mechanism. Alternatively or additionally, the association between Hcy and CVD may result from its metabolic precursor S-adenosyl-Hcy (SAH), or from the altered ratio of S-adenosylmethionine SAM/SAH. This competition is based on the known effects of these adenosylated metabolites on cellular methylation, disturbances of which may lead to endothelial dysfunction and/ or CVD. Thus, it is of great significance to know how these adenosylated metabolites (SAM, SAH) and Hcy are interrelated, and how they relate to CVD. We measured SAM, SAH, their molar ratio, and tHcy in plasma and in red blood cells (RBCs) of 30 patients with proven CVD (age 64.2  8.4) and 29 healthy controls (age 61  7.5). Plasma and RBCs SAM, SAH and tHcy levels were measured by HPLC method. We soon confirmed a significant increased of plasma levels of tHcy, SAM, and SAH in patients compared to the controls (13.1 vs. 10.9 micromol/l; 134 vs. 62.0 nmol/l; 79.2 vs. 24.0 nmol/l, respectively), while the molar ratio of SAM/SAH was decreased in patients (1.69 vs. 2.58). In RBCs patients exhibited increased levels of SAH compared with controls (325 vs. 201 nmol/l) whereas SAM (3327 vs. 3635 nmol/l) and the molar ratio of SAM/SAH (10.2 vs. 18.0) were significantly decreased. Folic acid and vitamin B12 in plasma were similar in patients and controls. We suppose that what we noticed might be due to the lack of remethylation in RBCs additionally to the inhibition of transmethylation reactions by elevation of SAH. Since the ratio of SAM/SAH is strongly linked with the activity of numerous enzymatic methylation reactions, these results suggest that methylation may be impaired in these patients. This increased intracellular SAH, when occurs in endothelial cells, would lead to excessive endothelial apoptosis, which is both pro-atherogenic and pro-thrombotic. Together, these results point out the importance of remethylation pathway in CVD.

Epidemiological evidence has revealed that hyperhomocysteinemia increases the risk for vascular disease. Methionine Synthase Reductase (MTRR) is one of several key enzymes in the homocysteine metabolic pathway and its mutant forms have been implicated in abnormal homocysteine accumulation. In this study, we determined total plasma homocysteine levels and MTRR A66G polymorphism in 114 patients with vascular disease: 58 patients with deep-vein thrombosis, 56 patients with arterial thrombosis, and 95 healthy subjects from the Sicilian population. Our data confirmed that, as already reported, moderately elevated t-Hcy levels are correlated with an increased risk of vascular disease. In our study, the levels of t-Hcy found in both deep-vein thrombosis (13.7+/-3.2 micromol/L) and arterial thrombosis (14.3+/-4.3 micromol/L) patient groups were higher than levels detected in normal subjects (8.7+/-2.7 micromol/L). We concluded that the MTRR A66G polymorphism was not associated with the t-Hcy plasma concentration because the same genotype frequency distribution was detected in both patients and healthy individuals.

A decrease of antioxidants, of neuroprotective and immunoregulatory vitamins and an increase of total-Homocysteine, Cholesterol, HDL-cholesterol, and of cellular stress markers [1] was reported in patients affected by Multiple Sclerosis. Recently, considering their unreliability, mainly due to the variability of the samples investigated, the attention focused on clinical relapse that results associated to a decrease of Uric acid and an increase of Cholesterol and stress markers. Aim. To identify the biochemical status during Multiple Sclerosis (MS) in a phase of clinical stability (PCS), we compared the blood levels of Urico acid (UA), Folic acid (FA), vitamins B12, A, and E, total-Homocysteine (t-Hcy), total Cholesterol (CHL) , HDL-CHL, and Triglycerides (TG) in 20 MS stable patients with those of 40 healthy controls. Methods. Consecutive MS patients, with relapsing-remitting or secondary-progressive courses, in a (PCS), were included. Plasma t-Hcy levels were determined by Ubbink method [1]. Technicon Immuno autoanalyser was used for serum FA and vitamin B12 assays. HPLC and fluorometry were used for UA, vitamin A and E, CHL, HDL-CHL, and TG assays. The ratio of E/CHL was valued. Results and Discussions. We found that MS patients in a PCS have higher blood levels of vitamin B12, t-Hcy, CHL, and HDL-CHL and lower blood levels of vitamin E and of the ratio E/CHL. The blood level of UA, FA, vitamin A, and TG do not differ from controls during this phase of MS. The increased level of CHL could be expression of both an its increased synthesis by neural cells and a chronic damage of myelin and axons. HDL-CHL concentration might arise to counteract the increase of CHL and assure its transport to the liver. Plasma levels of vitamin E, the major hydrophobic chain-breaking antioxidant, are decreased and our data confirm and support the view that it is consumed to counterbalance MS chronic neurodegeneration. Also, the increased levels of t-Hcy and vitamin B12 match previous studies performed in MS patients outside relapse. No significant differences in UA, FA, vitamin A, and TG levels appeared, making unprobable their involvement in the degenerative process of the stable phase of MS.