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PubMed2006

Vitamin B12 and vitamin B6 supplementation is needed among adults with phenylketonuria (PKU).

Phenylketonuria (PKU) is caused by an autosomal recessive deficiency of the enzyme phelnylalanine hydroxylase leading to a failure to convert phenylalanine to tyrosine. To avoid irreversible neurological damage because of increased phenylalanine, treatment is instituted rapidly after birth. We examined 31 adult PKU patients living on a less protein-restricted diet. Theoretically, these PKU patients had an increased risk of developing vitamin B(12) and B(6) deficiency because of a limited intake of animal products. Besides laboratory tests (n = 31) we obtained clinical information (n = 30) and detailed information on food consumption (n = 28). Three-quarters of the patients had early biochemical signs of vitamin B(12) deficiency. In spite of a normal folate status, 9 (29%) had a plasma homocysteine above 12 micromol/L. In accord with these findings, the food questionnaires indicated that 11 (39%) patients received less than the recommended daily vitamin B(12), and 20 (71%) received less vitamin B(6) than recommended. A significant association was found between reduced vitamin B(12) intake and both reduced serum cobalamins (p = 0.04) and reduced serum transcobalamin saturation (p = 0.03). Eleven patients took a vitamin pill daily, and these patients had a significantly lower plasma homocysteine compared to the rest. The present study suggests that adult PKU patients were at increased risk of developing vitamin B(12) deficiency, and their intake of vitamin B(6) was below the recommended daily intake. In conclusion PKU patients need continuing dietary guidance throughout adult life, and considering the risks, costs and potential benefits, daily vitamin supplementation seems justified in these patients.

Adolescent↗
PubMed1993

Prevention of vitamin K deficiency in infancy by weekly administration of vitamin K.

Vitamin K prophylaxis has been developed to prevent classic haemorrhagic disease of the newborn. Single vitamin K administration after birth has been reported to fail, resulting in late haemorrhagic disease of the newborn. The preventive effect of oral administration of vitamin K1 1 mg, repeated weekly during the first three months of life, was studied in 48 healthy breast-fed infants, by determination of thrombotest, PIVKA-II and vitamin K1 concentrations at the age of 4, 8 and 12 weeks. All infants showed normal thrombotest values and PIVKA-II was not detectable. Vitamin K1 concentrations were negatively correlated with the number of days elapsed since the most recent vitamin K administration. Six to seven days after the latest application, mean levels were 1223, 927 and 748 pg/ml at ages 4, 8 and 12 weeks, respectively. In conclusion, weekly administration of vitamin K1 1 mg offers complete protection against vitamin K deficiency and does not result in an accumulation of vitamin K1 in the blood.

Biomarkers↗
PubMed2002

Vitamin C and vitamin E antagonistically modulate human vascular endothelial and smooth muscle cell DNA synthesis and proliferation.

BACKGROUND: Vitamin C and E are suggested to play a preventive role in the pathogenesis of atherosclerosis. They reduce oxidation of low density lipoproteins (oxLDL), thereby protecting human vascular arterial endothelial and smooth muscle cells from oxLDL induced damages. AIMS OF THE STUDY: Since vascular arterial endothelial and smooth muscle cells are both involved in atherosclerotic plaque formation, we simultaneously examined the effect of vitamin C, E and oxLDL on their DNA synthesis and proliferation to further elucidate their joint role in this process. METHODS: Human umbilical arterial endothelial cells (HUAEC) and human arterial smooth muscle cells (HUASMC) were incubated with "preventive concentrations" of vitamin C (60 microM) and E (30 microM) and with LDL (60 microg/ml) of increasing oxidation grade. Cell proliferation and DNA synthesis were determined by cell count and [3H]-thymidine uptake, respectively. RESULTS: Vitamin C alone or in combination with E increased significantly cell number and [3H]-thymidine uptake in HUAEC. The combination exhibited the strongest effect. In contrast, cell number and [3H]-thymidine uptake in HUASMC were significantly decreased in the presence of vitamin C, vitamin E or its combination. OxLDL (60 microg/ml) inhibited cell number and [3H]-thymidine uptake in HUAECs, the latter in an oxidation-grade dependent manner. In HUASMC oxLDL promoted a higher cell number and [3H]-thymidine uptake. If induced by minimally oxLDL, this reduction or increase could be partially reversed by vitamin C alone or in combination with vitamin E. CONCLUSION: Vitamin C and E, alone or in combination, modulate proliferation and DNA synthesis of human arterial endothelial and muscle cells and this modulation is antagonistic. Thus, vitamin C and E may act "preventive" on atherosclerotic plaque formation in two steps: first reendothelialisation is promoted, then HUASMC growth is inhibited.

Antioxidants↗
PubMed1991

Modification of hepatic vitamin E stores in vivo. III. Vitamin E depletion by 1,2-dibromoethane may be related to initial conjugation with glutathione.

In the companion paper we demonstrated that hepatic vitamin E in rats becomes depleted and extrahepatic pools of vitamin E are altered by treatment with 1,2-dibromoethane (DBE). Vitamin E depletion may be dependent upon initial steps of DBE metabolism that are either oxidative (cytochrome P450 dependent) or conjugative (glutathione transferase dependent). That the liver content of glutathione (GSH) and vitamin E, the plasma concentration of vitamin E, and the serum activities of AST and ALT may be influenced by cytosolic metabolism of DBE was assessed by comparison of findings from rats treated with either 1,2-dichloroethane (DCE) or 1-bromo-2-chloroethane (BCE). The extent of oxidative metabolism was diminished by the use of tetradeutero-DBE (d4-DBE), and the availability of GSH for conjugative metabolism was diminished by pretreatment of rats with L-buthionine-S,R-sulfoximine (BSO) prior to treatment with DBE. Our results indicate that neither DCE nor BCE provokes a liver vitamin E depletion in rats, that d4-DBE treatment hastens but does not enhance the observed hepatic vitamin E depletion by comparison to animals treated with an equimolar dose of DBE, and that BSO pretreatment prevented the hepatic vitamin E depletion observed from animals treated with DBE alone. These results indicate that hepatic vitamin E depletion is the unique sequelae to conjugation of GSH with DBE, and we suggest the reactive episulfonium ion intermediate or a macromolecular adduct of this ion derived from DBE may play a role in liver vitamin E depletion associated with exposure to DBE.

Alanine Transaminase↗
PubMed1992

Effect of supplementation with folinic acid, vitamin B6, and vitamin B12 on valproic acid-induced teratogenesis in mice.

The effect of administration of folinic acid, vitamin B6 + vitamin B12, and their combination on valproic acid (VPA)-induced teratogenesis was studied in NMRI mice. VPA (500 mg/kg, sc) was injected on Day 8 of gestation and the vitamins (two dose levels) were injected ip 1 hr before, immediately before, and 1 hr after VPA administration. Folinic acid significantly reduced VPA-induced resorptions (21-24%), and palate, rib, and sternebral malformations. Exencephaly and spina bifida occulta were also reduced (14 and 40%, respectively), but the difference was not statistically significant. On the other hand, vitamin B6 + vitamin B12 significantly reduced VPA-induced exencephaly (23%), spina bifida occulta (80%), palate and rib malformations, kidney abnormalities, and fetal weight retardation. A combination of the three vitamins was effective in reducing VPA-induced exencephaly (23-30%), spina bifida occulta (60%), and palate and rib malformations. The protection against VPA-induced malformations was not complete and was not always dose related, and the reduction in exencephaly rate was only significant in the absence of a reduction in resorption rate. Full-length cleft palate, sternebral malformations, and retarded sternebral and caudal ossification were, however, increased by the high dose of combined vitamin administration. The present study supports the view that VPA-induced teratogenesis may be mediated via an interaction with folate metabolism. Although folinic acid and vitamin B6 + vitamin B12 can effectively reduce VPA malformations, the protection was not complete, which may suggest the involvement of other factors. Furthermore, the dose levels should be carefully chosen since high doses of the combined vitamins can actually increase the incidence of certain defects.

Abnormalities, Drug-Induced↗
PubMed2005

Clinical and laboratory safety of one year's use of a combination calcium + vitamin D tablet in ambulatory elderly women with vitamin D insufficiency: results of a multicenter, randomized, double-blind, placebo-controlled study.

OBJECTIVE: This article presents the results of an evaluation of the clinical and laboratory safety of a 1-year course of treatment with a combination calcium and vitamin D tablet in ambulatory women aged >65 years with vitamin D insufficiency. METHODS: In a multicenter, randomized, double-blind, placebo-controlled study conducted in France, women with a 25-hydroxyvitamin D level < or =12 ng/mL were randomized to receive either a combination tablet containing calcium carbonate 500 mg and vitamin D3 400 IU taken twice daily or a matching placebo tablet for 1 year. A complete clinical examination was performed at baseline and at 3, 6, 9, and 12 months of treatment; blood and urine samples were collected for laboratory analyses at the same time points. Safety was monitored based on adverse events recorded during the treatment period and on the results of laboratory tests, including measurement of creatinine and uric acid levels. RESULTS: The study included 192 women (mean [SD] age, 74.6 [6.9] years; mean weight, 64.0 [12.5] kg), 95 in the calcium + vitamin D group and 97 in the placebo group. Fifty women (21/95 [22.1%] calcium + vitamin D, 29/96 [30.2%] placebo) were prematurely withdrawn from the study for various reasons, with no difference in withdrawals between groups. Treatment-related adverse events were reported in 21 (22.1%) and 23 (24.0%) women in the respective treatment groups. These events consisted mainly of metabolic disorders (9 [9.5%] and 10 [10.4%], respectively), particularly hypercalcemia (6 [6.3%] and 8 [8.3%]) and gastrointestinal disorders (9 [9.5%] and 8 [8.3%]). No major complications directly related to calcium and vitamin D supplementation occurred during the course of treatment. Although renal function was not altered, the group who received calcium + vitamin D had significantly elevated concentrations of serum uric acid compared with those who received placebo (52.3% vs 37.2%; P = 0.046) but not urinary uric acid. CONCLUSIONS: In these ambulatory elderly women with vitamin D deficiency, supplementation with calcium + vitamin D appeared to be well tolerated over 1 year of treatment. No significant effects on creatinine clearance were observed. However, the proportion of women with elevated serum uric acid concentrations was significantly greater in those who received calcium + vitamin D compared with those who received placebo.

Aged↗
PubMed2004

Why "Vitamin D" is not a hormone, and not a synonym for 1,25-dihydroxy-vitamin D, its analogs or deltanoids.

Official nutrition committee reports in both North America and Europe now state that Vitamin D is more of a hormone than a nutrient. These statements are wrong, and do not reflect the definitions of either vitamin or hormone. Researchers often compound the problem by referring to calcitriol or other deltanoids as "Vitamin D". These things have serious consequences: (1) The literature is burdened by an ongoing confusion that presumes that the reader will somehow "know" what the writer refers to by "Vitamin D". (2) Medical practitioners not familiar with the ambiguities administer Vitamin D inappropriately when calcitriol or a deltanoid analog would be correct, or vice versa. (3) Attempts to promote Vitamin D nutrition are hindered by alarmist responses justifiably associated with the widespread administration of any hormone. Vitamin D is a vitamin in the truest sense of the word, because "insufficient amounts in the diet may cause deficiency diseases". The term, prohormone, is not relevant to the Vitamin D system, but 25-hydroxy-Vitamin D (calcidiol) is appropriately described as a prehormone, i.e. a glandular secretory product, having little or no inherent biologic potency, that is converted peripherally to an active hormone.

Terminology as Topic↗
PubMed2007

Circulating vitamin D3 and 25-hydroxyvitamin D in humans: An important tool to define adequate nutritional vitamin D status.

Circulating 25-hydroxyvitamin D [25(OH)D] is generally considered the means by which we define nutritional vitamin D status. There is much debate, however, with respect to what a healthy minimum level of circulation 25(OH)D should be. Recent data using various biomarkers such as intact parathyroid hormone (PTH), intestinal calcium absorption, and skeletal density measurements suggest this minimum level to be 80 nmol (32 ng/mL). Surprisingly, the relationship between circulating vitamin D(3) and its metabolic product-25(OH)D(3) has not been studied. We investigated this relationship in two separate populations: the first, individuals from Hawaii who received significant sun exposure; the second, subjects from a lactation study who received up to 6400IU vitamin D(3)/day for 6 months. Results (1) the relationship between circulating vitamin D(3) and 25(OH)D in both groups was not linear, but appeared saturable and controlled; (2) optimal nutritional vitamin D status appeared to occur when molar ratios of circulating vitamin D(3) and 25(OH)D exceeded 0.3; at this point, the V(max) of the 25-hydroxylase appeared to be achieved. This was achieved when circulating 25(OH)D exceeded 100 nmol. We hypothesize that as humans live today, the 25-hydroxylase operates well below its V(max) because of chronic substrate deficiency, namely vitamin D(3). When humans are sun (or dietary) replete, the vitamin D endocrine system will function in a fashion as do these other steroid synthetic pathways, not limited by substrate. Thus, the relationship between circulating vitamin D and 25(OH)D may represent what "normal" vitamin D status should be.

Cholecalciferol↗
PubMed2000

Bone tissue composition, dimensions and strength in female rats given an increased dietary level of vitamin A or exposed to 3,3',4, 4',5-pentachlorobiphenyl (PCB126) alone or in combination with vitamin C.

In previous studies we have described structural and functional changes in rat bone tissue caused by 3,3',4,4',5-pentachlorobiphenyl (PCB126). Some of the effects caused by PCB126 resemble those found in vitamin C-deficient rats, as well as those found in rats with a high dietary intake of vitamin A. The present investigation was designed to determine if these PCB126-induced changes could be inhibited by addition of vitamin C to the drinking water and if they could be evoked by vitamin A administration. Five groups of female rats were used in this study, which lasted for 12 weeks. Three of the groups were exposed to PCB126 (total dose 320 microgram/kg, bw), either alone or in combination with vitamin C added to the drinking water (1 and 10 g/l, respectively). One group was given feed with increased level of vitamin A (600000 U/kg pellet) and the fifth group served as controls. Using peripheral quantitative computed tomography (pQCT), it was found that PCB126 increased trabecular density and cortical thickness, but reduced the trabecular area. Furthermore, maximum torque and stiffness of the humerus during torsional testing and serum osteocalcin levels were reduced by PCB126. Of the PCB126 induced effects observed, addition of vitamin C only inhibited the reduction of serum osteocalcin. Like PCB126 vitamin A supplementation increased the inorganic content and the bone density and also reduced the trabecular area and polar moment of inertia but did not increase the cortical thickness or reduce maximum torque, stiffness or serum osteocalcin level. Apparently, the effects induced by PCB126 are not mediated either via decreased vitamin C level or increased vitamin A level.

Animals↗
PubMed1999

Glutamyl substrate-induced exposure of a free cysteine residue in the vitamin K-dependent gamma-glutamyl carboxylase is critical for vitamin K epoxidation.

The vitamin K-dependent carboxylase catalyzes the posttranslational modification of glutamic acid to gamma-carboxyglutamic acid in the vitamin K-dependent proteins of blood and bone. The vitamin K-dependent carboxylase also catalyzes the epoxidation of vitamin K hydroquinone, an obligatory step in gamma-carboxylation. Using recombinant vitamin K-dependent carboxylase, purified in the absence of propeptide and glutamic acid-containing substrate using a FLAG epitope tag, the role of free cysteine residues in these reactions was examined. Incubation of the vitamin K-dependent carboxylase with the sulfhydryl-reactive reagent N-ethylmaleimide inhibited both the carboxylase and epoxidase activities of the enzyme. This inhibition was proportional to the incorporation of radiolabeled N-ethylmaleimide. Stoichiometric analyses using [(3)H]-N-ethylmaleimide indicated that the vitamin K-dependent carboxylase contains two or three free cysteine residues. Incubation with propeptide, glutamic acid-containing substrate, and vitamin K hydroquinone, alone or in combination, indicated that the binding of a glutamic acid-containing substrate to the carboxylase makes accessible a free cysteine residue that is important for interaction with vitamin K hydroquinone. This is consistent with our previous observation that binding of a glutamic acid-containing substrate activates vitamin K epoxidation and supports the hypothesis that binding of the carboxylatable substrate to the enzyme results in a conformational change which renders the enzyme catalytically competent.

Amino Acid Sequence↗
PubMed2004

Sequential versus combined treatment of human breast cancer cells with antiestrogens and the vitamin D analogue EB1089 and evaluation of predictive markers for vitamin D treatment.

Development of resistance to antihormonal therapy is a major problem in the treatment of breast cancer patients. Metastatic tumors, which progress after a period of response to treatment, often respond to second line endocrine treatment, but eventually develop estrogen independent growth. Vitamin D analogues are promising new drugs, using alternative mechanisms to inhibit growth of breast cancer cells. The sensitivity to antiestrogens and vitamin D analogues has been proposed to be inverse, indicating that the sensitivity to vitamin D analogues might increase after development of antiestrogen resistance and vice versa. In this study, the inverse sensitivity between antiestrogens and the vitamin D analogue EB1089 was examined in antiestrogen and vitamin D resistant breast cancer cell lines. The majority of the investigated antiestrogen resistant cell lines had increased sensitivity to treatment with the vitamin D analogue EB1089. In addition, growth of a vitamin D resistant cell line was more inhibited by the pure antiestrogen ICI 182,780 than the growth of the parental cells, indicating that the compounds may be used sequentially. An association between the expression level of the vitamin D receptor (VDR) and EB1089 sensitivity was observed, suggesting that VDR is a possible predictive marker for response to vitamin D treatment. Valuation of Bcl-2 gene expression may be useful in combination with VDR to predict the outcome of treatment with EB1089. Furthermore, we observed a synergistic growth inhibition and an abrogated development of resistance upon combined treatment with ICI 182,780 and EB1089. Therefore, antiestrogens and vitamin D analogues may also be used as combined treatment for breast cancer patients in the future.

Antineoplastic Agents↗
PubMed1996

Effect of dietary vitamin C on compression injury of the spinal cord in a rat mutant unable to synthesize ascorbic acid and its correlation with that of vitamin E.

The roles of vitamin C on secondary pathological changes after spinal cord injury were investigated by evaluating the effects of dietary vitamin C on experimental spinal cord injury in a mutant strain of Wistar rats unable to synthesize ascorbic acid (ODS rats). Two groups of ODS rats were given vitamin C-deficient or vitamin C-supplemented diet for 1 week before injury. Motor disturbance induced by spinal cord injury was found to be greater in the vitamin C-deficient group. Histologically, the area of bleeding in the spinal cord was also greater in the vitamin C-deficient group. The levels of ascorbic acid and alpha-tocopherol in the spinal cord tissue and serum decreased during and after compression injury of the spinal cord. The decrease of alpha-tocopherol was similar in the two groups. However, the decrease of ascorbic acid was greater in the vitamin C-supplemented group. These results indicated that their protective effects against spinal cord injury are through scavenging water-soluble free radicals by vitamin C and lipid-soluble by vitamin E, and the effects of these vitamins were suggested to be independent.

Animals↗
PubMed1999

Modification of the nutrition questionnaire for elderly to increase its ability to detect elderly people with inadequate intake of energy, calcium, vitamin C and vitamin D.

OBJECTIVE: To validate the Nutrition Questionnaire for Elderly (NQE) aimed at health care personnel -and develop and validate a modified version of the questionnaire (MNQE) to improve its sensitivity in detecting elderly people with inadequate intake of specific nutrients and energy. DESIGN: The NQE was used to rank the nutrient intake of participants as 'acceptable' (OK-->) or 'at risk' (OBS-->) with respect to energy, calcium, vitamin C and vitamin D--nutrients with a high risk of deficiency, especially among the homebound or institutionalised elderly. The sensitivity, specificity and predictive capacity were calculated by means of a 4 d estimated record (study 1). Based on the results minor adjustments of the NQE was made, and the already obtained information was used to assess the theoretical validity of the MNQE (study 2). Finally the MNQE was validated in a new population (study 3). SETTING AND SUBJECTS: Ninety-five old people ( > 65 y) living in nursing-homes (Bagsvaerd or Havdrup), or at home in the same home-care district (Valby) or in the same preventive home-visit district (Rødovre) were recruited. Excluded were those who declined to participate or who were in a terminal condition (n = 3). RESULTS: The sensitivity of the NQE regarding the intakes of energy, calcium, vitamin C and vitamin D was quite low (respectively 0.46, 0.08, 0.05 and 0.38) (study 1). However minor adjustments of the NQE increased the sensitivity both in theory (energy: 0.64, calcium: 0.95, vitamin C: 1.00 and vitamin D: 0.84) (study 2) and in practice (energy: 1.00, calcium: 0.40, vitamin C: 0.86 and vitamin D: 0.85) (study 3). Modification of the NQE did not reduce the high specificity and predictive capacity of the original version. CONCLUSIONS: Modifications of the NQE resulted in a questionnaire with a high sensitivity, specificity and predictive capacity for detecting inadequate intake of energy, calcium, vitamin C and vitamin D in elderly people.

Aged↗
PubMed1979

No strict coupling of vitamin K1 (2-methyl-3-phytyl-1,4-naphthoquinone)-dependent carboxylation and vitamin K1 epoxidation in detergent-solubilized microsomal fractions from rat liver.

NAD(P)H dehydrogenase ('DT-diaphorase', EC 1.6.99.2) and vitamin K epoxidase were removed by affinity chromatography from detergent-solubilized microsomal fractions. Thereby the microsomal fractions normally carrying out vitamin K1-dependent carboxylation of the microsomal precursor proteins of the prothrombin complex were inactivated. Purified NAD(P)H dehydrogenase added to this system restored carboxylation in the presence of vitamin K1 (2-methyl-3-phytyl-1,4-naphthoquinone) plus NADH. Vitamin K1 hydroquinone (2-methyl-3-phytyl-1,4-naphthoquinol) had no effect, in contrast with its effect in the intact system, where it can substitute for vitamin K1 plus NADH. The ability of NAD(P)H dehydrogenase to restore carboxylation in a system without vitamin K epoxidase activity shows that there is no obligatory coupling of the vitamin K1-dependent carboxylation with vitamin K1 epoxidation. These results suggest that the form of vitamin K1 that is active in the carboxylation reaction can be produced independently in two reactions: by NAD(P)H dehydrogenase in the reduction of the quinone and by vitamin K epoxidase in the epoxidation of the hydroquinone.

Animals↗
PubMed1998

Biosynthesis of vitamin B12 in anaerobic bacteria--experiments with Eubacterium limosum on the transformation of 5-hydroxy-6-methyl-benzimidazole, its nucleoside, its cobamide, and of 5-hydroxybenzimidazolylcobamide in vitamin B12.

In anaerobic bacteria 5-hydroxybenzimidazole and 5-hydroxy-6-methylbenzimidazole are precursors of the 5,6-dimethylbenzimidazole moiety of vitamin B12. In order to elucidate the pathway from these bases to vitamin B12, experiments on the transformation of 5-hydroxy-6-methylbenzimidazole, of 5-hydroxy-6-methylbenzimidazole-alpha-D-ribofuranoside, of 5-hydroxybenzimidazolylcobamide and of 5-hydroxy-6-methylbenzimidazolylcobamide into vitamin B12 were carried out. The vitamin B12 synthesized by the anaerobe Eubacterium limosum in the presence of 5-hydroxy-6-methylbenzimidazole and L-[methyl-13C]methionine was subjected to NMR spectroscopy. It revealed that the methyl group at C5 of the 5,6-dimethylbenzimidazole moiety was 13C labeled, whereas the methyl group at C6 was unlabeled. This shows that the transformation of 5-hydroxy-6-methylbenzimidazole into the base moiety of vitamin B12 occurs regiospecifically. 5-Hydroxy-6-methylbenzimidazole-alpha-D-ribofuranoside as well as 5-hydroxybenzimidazolylcobamide and 5-hydroxy-6-methylbenzimidazolylcobamide were also transformed into vitamin B12 by E. limosum. When 5-hydroxy-6-methylbenzimidazolylcobamide 13C labeled at C2 of the base part and 14C labeled in the ribose was used for this experiment, the vitamin B12 obtained from this cobamide was 13C and 14C labeled in the same positions. This demonstrates that the alpha-glycosidic bond of the precursor cobamide is not split during the formation of vitamin B12. It can be deduced from these results that the precursor bases are transformed regiospecifically into their alpha-nucleotides, and partially into their cobamides. The alpha-nucleotides are then transformed into alpha-ribazole-5'-phosphate and, subsequently, into vitamin B12. Most likely the cobamides are degraded to the alpha-nucleotides before being used for the biosynthesis of vitamin B12. A pathway for the latter process is suggested.

Benzimidazoles↗
PubMed2000

Water-soluble vitamin levels in patients undergoing high-flux hemodialysis and receiving long-term oral postdialysis vitamin supplementation.

The prescription of multivitamin supplements for dialysis patients is routine practice, but the doses prescribed differ greatly from one dialysis center to another. Few data are available concerning long-term vitamin supplementation and its effects on patients either on high-flux hemodialysis or receiving postdialysis supplementation. For several years, we have systematically prescribed to our patients an oral postdialysis multivitamin supplement containing thiamine hydrochloride 100 mg, riboflavin 20 mg, pyridoxine hydrochloride 50 mg, folic acid 6 mg, and ascorbic acid 500 mg. The aim of this study was to perform a cross-sectional long-term evaluation of the vitamin levels in patients who received this vitamin supplement for at least 12 months. We also were interested in investigating the plasma oxalic acid and total homocysteine levels associated with the long-term prescription of these vitamin supplements. Thirty-three patients on high-flux dialysis were studied. Vitamin levels and/or vitamin-dependent enzymatic activities were within the normal range (N) in all patients. The mean results (+/-SD) were plasma ascorbic acid 13.6 +/- 6.4 mg/L (N > 4), plasma folate 14.1 +/- 1.1 microg/L (N > 3), for vitamin B1, alpha-ETK 1.02 +/- 0.02 (N < 1.18) and ETKo 100 +/- 13 U/L (N > 70), for vitamin B2, alpha-EGR 1.00 +/- 0.07 (N < 1.52) and EGRo 1282 +/- 213 U/L (N > 672), and for vitamin B6, alpha-EGOT 1.34 +/- 0.10 (N < 1.8) and EGOTo 380 +/- 84 U/L (N > 228). Plasma oxalic acid was higher than normal in all patients (mean = 61 +/- 15 micromol/L, N < 33). However, all patients had oxalic acid levels within the range reported in the literature for patients not taking extra ascorbic acid. Mean total homocysteine was 24 +/- 8 micromol/L with only 4 patients (12%) having normal levels (N < 15). In conclusion, the postdialysis supplement given provides adequate vitamin levels in almost all patients in the long term. Postdialysis prescription allows an optimal compliance with the treatment, is well accepted by the patients, and is cost-effective.

Adult↗
PubMed1995

Mutagenesis of vitamin K-dependent carboxylase demonstrates a carboxyl terminus-mediated interaction with vitamin K hydroquinone.

The gamma-glutamyl carboxylase and vitamin K epoxidase activities of a series of mutants of bovine vitamin K-dependent carboxylase with progressively larger COOH-terminal deletions have been analyzed. The recombinant wild-type (residues 1-758) and mutant protein carboxylases, Cbx 711, Cbx 676, and Cbx 572, representing residues 1-711, 1-676, and 1-572, respectively, were expressed in baculovirus-infected Sf9 cells. Wild-type carboxylase had a Km for the substrate Phe-Leu-Glu-Glu-Leu (FLEEL) of 0.87 mM; the carboxylation of FLEEL was stimulated 2.5-fold by proPT18, the propeptide of prothrombin. Its Km for vitamin K hydroquinone was 23 microM and the specific epoxidase activity of the carboxylase was 938 pmol vitamin KO/30 min/pmol of carboxylase. Cbx 711, which was also stimulated by proPT18, had a Km for FLEEL, a Km for vitamin K hydroquinone, and a specific epoxidase activity that was comparable to the wild-type carboxylase. In contrast Cbx 572 lacked both carboxylase and epoxidase activities. Although Cbx 676 had a normal carboxylase active site in terms of the Km for FLEEL and its stimulation by proPT18, the Km for vitamin K hydroquinone was 540 microM, and the specific epoxidase activity was 97 pmol KO/30 min/pmol of Cbx 676. The catalytic efficiencies of Cbx 676 for glutamate carboxylation and vitamin K epoxidation were decreased 15- and 400-fold, respectively, from wild-type enzyme reflecting the requirement for formation of an activated vitamin K species for carboxylation to occur. These data indicate that the truncation of COOH-terminal segments of the carboxylase had no effect on FLEEL or propeptide recognition, but in the case of Cbx 676, selectively affected the interaction with vitamin K hydroquinone and the generation of epoxidase activity. These data suggest that a vitamin K epoxidase activity domain may reside near the COOH terminus while the carboxylase active site domain resides toward the NH2 terminus.

Amino Acid Sequence↗
PubMed2002

Protective role of melatonin and a combination of vitamin C and vitamin E on lung toxicity induced by chlorpyrifos-ethyl in rats.

The ameliorating effects of melatonin and vitamin C plus vitamin E were examined histologically and biochemically in lung tissues in rats exposed to chlorpyriphos-ethyl (CE). Experimental groups were as follows: Control group (C), CE treated group (CE), vitamin C plus vitamin E treated group (Vit), melatonin treated group (Mel), vitamin C plus vitamin E plus CE treated group (Vit + CE), and melatonin plus CE treated group (Mel + CE). Vitamin E and vitamin C were administered intramuscularly at the rates of 150 and 200 mg per kg body weight, respectively, in Vit and Vit + CE groups, once a day for 6 consecutive days. Melatonin was administered intramuscularly at the rate of 10 mg per kg body weight in Mel and Mel + CE groups, once a day for 6 consecutive days. At the end of the fifth day, the rats of CE, Vit + CE and Mel + CE groups were treated orally with CE dissolved in corn oil with two equal doses of 41 mg CE per kg body weight at zero and twenty-first hours. Tissue samples of lungs were taken by using appropriate techniques for biochemical and histological examinations under anesthesia at the twenty-fourth hours of CE administration, at the end of the sixth day of the experiment. In tissue homogenates, the level of thiobarbituric acid reactive substances (TBARS), antioxidant potential (AOP), and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were determined. TBARS was significantly high (p < 0.05) in CE group compared to control group, while TBARS was found to significantly decrease (p < 0.05) with Vit and Mel groups compared to control. On the other hand, TBARS was seen to significantly decrease (p < 0.05) in both groups of Vit + CE and Mel + CE compared to CE group. In comparison with CE group, SOD activity was significantly high (p < 0.05) with the groups of Vit, Mel, Vit + CE and Mel + CE. GSH-Px activity was found to significantly decrease (p < 0.05) with CE group, compared with both C and Vit groups. AOP was significantly lower (p < 0.01) in CE group than C group. Although there was an increased AOP with Vit + CE and Mel + CE groups compared to CE group, the increase in AOP was only seen to be significant (p < 0.05) in Mel + CE group. In comparison with C group, AOP significantly (p < 0.05) increased with Vit group. There was also a significant (p < 0.05) increase in AOP with Mel + CE group, compared with CE group. Additionally, AOP was significantly lower (p < 0.05) in Vit + CE group than Mel + CE group. Lungs were examined histologically at the end of sixth day. There were remarkable changes in the histomorphology of peribronchial and perivascular area in the lung of rats treated with CE. These were infiltration of mononuclear cells (such as lymphocytes, plasmocytes, macrophages), hyperplasia of type II pneumocyte, and thickened and increased connective tissue. Damage to the lung tissue such as increased inflammatory mononuclear cells in peribronchial and perivascular areas were more pronounced for the CE group than Vit + CE and Mel + CE groups in which these changes were higher than C, Vit and Mel groups. These results suggest that CE increases lipid peroxidation and decreases antioxidant enzymes activities and AOP due to increasing oxidative stress induced by CE, and high doses of vitamin C plus vitamin E and melatonin considerably reduce CE toxicity in lung tissues of rats.

Animals↗