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At least 253 records · Page 14Linked to original sources
PubMed2003

Vitamin B-12 metabolism in HIV-infected patients in the age of highly active antiretroviral therapy: role of homocysteine in assessing vitamin B-12 status.

BACKGROUND: Before the advent of highly active antiretroviral therapy (HAART), 20% and 10% of HIV-infected patients had low vitamin B-12 and red blood cell folate (RBCF) concentrations, respectively. However, few patients had real vitamin B-12 deficiency. OBJECTIVE: We evaluated the prevalence of low vitamin B-12 and RBCF concentrations in HIV-infected patients receiving HAART and the usefulness of serum homocysteine (sHcy) for differentiating patients with deficiency from those with harmlessly low vitamin B-12. DESIGN: The prevalence of low vitamin B-12 and RBCF was evaluated in 126 HIV-infected patients receiving HAART. Moreover, sHcy concentrations were evaluated in 40 HIV-infected patients with low vitamin B-12 and in 37 HIV-infected patients with low RBCF and were compared with those in 128 HIV-infected patients with normal vitamin B-12 and RBCF. sHcy was used to monitor treatment with vitamin B-12 and folic acid in 28 patients (24 with low vitamin B-12 and RBCF and 4 with hyperhomocysteinemia but normal vitamin B-12 and RBCF). RESULTS: The prevalence of low vitamin B-12 was significantly lower in patients receiving HAART than in previously studied patients who did not receive HAART (8.7% compared with 27%). Nine of the 40 patients (22.5%) with low vitamin B-12 (< or = 200 pmol/L) had hyperhomocysteinemia (> 17.5 micromol homocysteine/L). Nineteen (51.4%) of the 37 patients with low RBCF (< or = 580 nmol/L, percentile 10) had hyperhomocysteinemia. Among the 9 patients with an RBCF concentration < or = 450 nmol/L (percentile 2.5), all had hyperhomocysteinemia. The treatment with vitamin B-12 and folic acid normalized sHcy concentrations. CONCLUSIONS: The prevalence of low vitamin B-12 decreased after the introduction of HAART. The study of sHcy is useful for detecting HIV-infected patients with low vitamin B-12 and real deficiency.

Adult↗
PubMed1994

The vitamin A and vitamin E status of horses raised in Alberta and Saskatchewan.

The purpose of the study was to determine normal baseline levels of vitamin A and vitamin E in clinically normal horses under typical field conditions in Saskatchewan and Alberta. Heparinized blood samples were collected from approximately 400 clinically healthy horses selected from 24 locations in Alberta and Saskatchewan during a two-year period. For each horse, historical information including feed type, vitamin supplementation, time of year, sex, and age were recorded. From each blood sample, the plasma vitamin A (all-transretinol) and vitamin E (alpha-tocopherol) levels were measured using high pressure liquid chromatography. Normal baseline plasma vitamin A and vitamin E concentrations recorded during the study were 0.70 mumol/L and 7.65 mumol/L, respectively. The plasma vitamin concentrations were lower in the younger horses. The plasma vitamin levels were higher from May to August, as compared to other times of the year. Horses grazing fresh pasture exclusively during the summer months had plasma vitamin A and vitamin E concentrations that were 27% and 63% greater than horses fed harvested or stored feeds during the same time period. Sex-related differences were not evident in the study. A number of factors may influence the baseline plasma vitamin A and vitamin E levels in horses. Consequently, it is unadvisable to use a single evaluation to assess vitamin status. Multiple sampling from individual horses or sampling from many horses within a herd may reduce the variability and improve the ability to monitor vitamin status from plasma submissions.

Age Factors↗
PubMed1982

Vitamin D from skin: contribution to vitamin D status compared with oral vitamin D in normal and anticonvulsant-treated subjects.

1. The plasma 25-hydroxycholecalciferol [25-(OH)D3] response to measured u.v. irradiation applied thrice weekly for 10 weeks was investigated in normal and in anticonvulsant-treated subjects. 2. Levels of plasma 25-(OH)D3 achieved after u.v. irradiation were similar in both normal and anticonvulsant-treated subjects, suggesting that hepatic microsomal enzyme induction does not lead to low plasma 25-(OH)D3 concentrations. 3. Cholecalciferol was present in plasma of normal subjects in a very low concentrations (less than 5.0 nmol/l) and did not increase until plasma 25-(OH)D3 levels exceeded 62.5 nmol/l. 4. Cholecalciferol occurred in significant concentrations in plasma during whole body u.v. irradiation or during oral dosage of 62.5 nmol (100 i.u) or more daily. 5. Plasma 25-(OH)D3 concentrations reached a steady state after 5-6 weeks of u.v. irradiation or of oral intake within the usual intake range. 6. Cholecalciferol synthesis in skin calculated from the steady-state equation was 0.0015 +/- 0.0008 nmol/mJ. 7. Cholecalciferol synthesis in skin was also calculated from the oral dosage required to yield the same plasma 25-(OH)D3 concentration as u.v. irradiation and was 0.0024 +/- 0.0018 nmol/mJ. 8. Rates of cholecalciferol synthesis calculated from these data suggest that many of the population of England receive insufficient u.v. irradiation to maintain vitamin D status throughout the year.

Adolescent↗
PubMedDate not supplied

Effects of different levels of vitamin C intake on the vitamin C concentration in guinea pigs plasma and the effect of vitamin C intake on anaphylaxis.

The plasma ascorbate level after a single intraperitoneal dose of 25, 100 or 250 mg Na-ascorbate was followed up in vivo over a period of 24 hours. Intraperitoneal administration of Na-ascorbate caused a rapid increase of ascorbic acid plasma concentration. Maximum ascorbic acid plasma level was obtained 30 minutes after parenteral administration of the test dose. No great difference was found between the 12- and 24-hour ascorbic acid plasma values. The effect of Na-ascorbate on fatal anaphylaxis was also investigated in 18 guinea pigs. The animals treated with 281 mg/day Na-ascorbate rarely developed anaphylactic shock or the shock was of weaker intensity. Mortality was reduced from 40% (control group) to 11% when Vitamin C was given for four days before and one day after passive transfer of rabbit anti-HGG (human gamma globulin) antibody. A possible protective role of ascorbic acid by preventing anaphylaxis is discussed. Passive administration of ascorbic acid was found to protect guinea pigs from fatal anaphylaxis.

Anaphylaxis↗
PubMed2002

In vitro manipulations of vitamin C and vitamin E concentrations alter intracellular O2- production of hybrid striped bass (Morone chrysops x Morone saxatilis) head-kidney cells.

To examine the mechanism by which vitamins C and E alter phagocyte function, a series of in vitro manipulations were conducted with cells isolated from the head-kidney of hybrid striped bass (average weight 680 g) fed a diet supplemented with minimum requirement levels of vitamins C and E for 2 weeks. Head-kidney phagocytes were cultured in media containing physiologically deficient (23 microM, adequate (45 microM) or excessive (182 microM) concentrations of vitamin C, and physiologically deficient (5 microM), adequate (9 microM) or excessive (32 microM) concentrations of vitamin E for 18 h. Following culture and stimulation, levels of reactive oxygen intermediates and hydrogen peroxide were determined. There were no effects of vitamin C or vitamin E concentrations on hydrogen peroxide or extracellular O2- generation. Intracellular O2- production, however, was significantly (P < or = 0.05) affected. When vitamin C was supplied at deficient levels to the medium, vitamin E elevated O2- production to levels not different from those of cells incubated with requirement levels of both vitamins. Similarly, when vitamin E was deficient in the media, vitamin C supplementation at requirement levels normalised intracellular O2- production. This data provides support for the presence of a vitamin C and vitamin E sparing mechanism in phagocytic head-kidney cells of hybrid striped bass and yield some insight into the mechanisms by which vitamin C and vitamin E function in immunomodulation.

Animals↗
PubMed1991

On the problematic nature of vitamin E requirements: net vitamin E.

The requirement for vitamin E is closely related to the dietary intake of polyunsaturated fatty acids (PUFA). By the protective mechanism to prevent PUFA from being peroxidized, vitamin E is metabolically consumed. In addition, PUFA impair the intestinal absorption of vitamin E. Therefore PUFA generate an additional vitamin E requirement on the order of 0.6, 0.9, 1.2, 1.5, and 1.8 mg vitamin E (RRR-alpha-tocopherol-equivalents), respectively, for 1 g of dienoic, trienoic, tetraenoic, pentaenoic, and hexaenoic acid. For this reason, the gross vitamin E content of food containing PUFA does not allow an evaluation of this food as a source of vitamin E. A suitable measure is the net vitamin E content, i.e., gross vitamin E minus the amount needed for PUFA protection. Therefore, some food-stuffs generally considered as vitamin-E sources, as concluded from their gross vitamin E content, cause in reality a vitamin E deficiency if not sufficiently compensated by other vitamin E supplying food constituents. Examples of the net vitamin E content of some fats and oils, fish and nuts are shown. Consequences for food composition data and food labeling and the problem of meeting the vitamin-E requirements are discussed.

Dietary Fats, Unsaturated↗
PubMed2001

Effect of vitamin E and vitamin C on the DNA synthesis of human umbilical arterial endothelial cells.

BACKGROUND: Endothelial cell growth and reendothealization after vascular injury protect the vessel wall against endothelial dysfunction which is believed to play a major role in the pathogenesis of atherosclerosis. AIM: of the study To investigate a possible protective role of antioxidant vitamins in the present study, the effect of vitamin E (alpha-tocopherol) alone and in combination with vitamin C on the DNA synthesis of human umbilical arterial endothelial cells (HUAEC) was examined. Furthermore, because oxidized low-density lipoprotein (ox-LDL) is thought to be involved in atherogenesis, the combined effect of vitamin E and vitamin C with ox-LDL and the influence of vitamin-pretreated LDL on HUAEC proliferation were investigated. METHODS: DNA-synthesis was determined by measurement of [3H]thymidine incorporation into the cell DNA. RESULTS: Vitamin E alone and in combination with vitamin C resulted in an increase in [3H]thymidine incorporation into cell DNA, especially in the presence of basic fibroblast growth factor (bFGF). All vitamin-pretreated LDL samples and ox-LDL led to a nearly complete inhibition of endothelial DNA-synthesis. The ox-LDL-induced effect could not be prevented by vitamin E alone nor in combination with vitamin C. CONCLUSIONS: It seems that once LDL oxidation is in process, vitamin E alone and in combination with vitamin C is ineffective to exert its antioxidative capacity under the conditions used. Thus, vitamin E alone and combined with vitamin C may act as antiatherogens by inducing endothelial cell growth.

Antioxidants↗
PubMed1992

Elevation of blood vitamin D2 levels does not impede the release of vitamin D3 from the skin.

The mechanism for the transfer of fat-soluble vitamin D3 from the avascular basal cellular layers of the epidermis to dermal capillaries and peripheral circulation is unknown, although vitamin D-binding protein (DBP) is thought to mediate this process. To evaluate the effect of increased occupancy of vitamin D carrier(s) on vitamin D3 removal from the skin, serial serum vitamin D2 and D3 concentrations were determined in three groups of six healthy volunteers given combinations of an oral dose of vitamin D2 (50,000 IU) and a fixed dose of UVB radiation (27 mJ/cm2). Serum vitamin D3 levels increased significantly following UVB (time effect, P < .01 by ANOVA), but the response remained unchanged after pretreatment with vitamin D2, increasing from 3 +/- 1 to 14 +/- 5 ng/mL (mean +/- SEM), versus UVB alone, 5 +/- 1 to 16 +/- 5 ng/mL. Elevation of serum vitamin D2 levels was also similar in the groups given vitamin D2 alone (< 1 to 64 +/- 8 ng/mL) and vitamin D2 + UVB (< 1 to 45 +/- 8 ng/mL). There was no time or treatment effect for changes in serum levels of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, or (DBP) levels (P > .1). We conclude that vitamin D3 egress from the skin is not affected by elevated circulating vitamin D concentrations; thus, the cutaneous release of vitamin D is probably mediated by a protein such as DBP with a high carrying capacity for the vitamin.

Administration, Oral↗
PubMed2003

Vitamin C and vitamin E restore the resistance of GSH-depleted lens cells to H2O2.

A decline in reduced glutathione (GSH) levels is associated with aging and many age-related diseases. The objective of this study was to determine whether other antioxidants can compensate for GSH depletion in protection against oxidative insults. Rabbit lens epithelial cells were depleted of > 75% of intracellular GSH by 25-200 microM buthionine sulfoximine (BSO). Depletion of GSH by BSO alone had little direct effect on cell viability, but resulted in an approximately 30-fold increase in susceptibility to H(2)O(2)-induced cell death. Experimentally enhanced levels of nonprotein sulfhydryls other than GSH (i.e., N-acetylcysteine) did not protect GSH-depleted cells from H(2)O(2)-induced cell death. In contrast, pretreatment of cells with vitamin C (25-50 microM) or vitamin E (5-40 microM), restored the resistance of GSH-depleted cells to H(2)O(2). However, concentrations of vitamin C > 400 microM and vitamin E > 80 microM enhanced the toxic effect of H(2)O(2). Although levels of GSH actually decreased by 10-20% in cells supplemented with vitamin C or vitamin E, the protective effects of vitamin C and vitamin E on BSO-treated cells were associated with significant ( approximately 70%) decreases in oxidized glutathione (GSSG) and concomitant restoration of the cellular redox status (as indicated by GSH:GSSG ratio) to levels detected in cells not treated with BSO. These results demonstrate a role for vitamin C and vitamin E in maintaining glutathione in its reduced form. The ability of vitamin C and vitamin E in compensations for GSH depletion to protect against H(2)O(2)-induced cell death suggests that GSH, vitamin C, and vitamin E have common targets in their actions against oxidative damage, and supports the preventive or therapeutic use of vitamin C and E to combat age- and pathology-associated declines in GSH. Moreover, levels of these nutrients must be optimized to achieve the maximal benefit.

Animals↗
PubMed2005

Differential response of plasma and immune cell's vitamin E levels to physical activity and antioxidant vitamin supplementation.

OBJECTIVE: To assess the differential response of plasma, lymphocyte and neutrophil vitamin E levels to high-intensity physical activity and to vitamin C and E supplementation. SUBJECTS: In all, 14 male trained amateur runners (32-36 y old) were randomly divided in two groups (supplemented and placebo), and participated in a half marathon race. The subjects did not take any other supplements than the ones provided for this study. INTERVENTION: Vitamin C (152 mg/day) and E (50 mg/day) supplementation was administrated to athletes for a month, using a new almond-based isotonic and energetic beverage (supplemented group). The usual dietary habits of participants were assessed using a self-reported 7-day 24-h recall before the day of the study. To avoid the beverage influence, nonenriched vitamin C and E almond-based isotonic and energetic beverage was given to the placebo group. After 1 month, subjects participated in a half marathon race (21 km run). Vitamin E concentration was determined in plasma, neutrophils and lymphocytes before and immediately after the race, and 3 h after finishing the race. RESULTS: Daily energy intake and caloric profile of supplemented and placebo group were not different except for vitamin C and E supplementation. Vitamin supplementation and exercise had no effect on vitamins E levels in plasma. The exercise significantly (P<0.05) increased the lymphocyte vitamin E concentration both in the placebo (+119%) and supplemented groups (+128%), and neutrophil vitamin E content in the supplemented group (+88%). These levels remained significantly (P<0.05) high after the short recovery. After exercise, vitamin E levels in lymphocytes and neutrophils of supplemented subjects were practically twice the levels before exercise, whereas neutrophil vitamin E content of the placebo group was close to those in plasma. CONCLUSION: After endurance exercise, lymphocytes increased their vitamin E content in the supplemented and placebo subjects whereas this trend in neutrophils was just observed in the supplemented group. The determination of vitamin E content in lymphocytes and neutrophils after exercise is a useful tool to assess the functional status of vitamin E.

Adult↗
PubMed2001

Vitamin A intake affects the contribution of chylomicrons vs. retinol-binding protein to milk vitamin A in lactating rats.

To investigate the influence of vitamin A intake on the contribution of chylomicrons vs. holo retinol-binding protein to milk vitamin A, female rats were fed diets containing either 10 (n = 6) or 50 micromol vitamin A/kg body (n = 4) during pregnancy and through d 13 of lactation. [3H]Vitamin A was incorporated into each diet beginning on d 6 of lactation. Vitamin A concentrations on d 13 were significantly higher in dam liver (x 3), pup liver (x 2.6), milk (x 2.5) and mammary tissue (x 1.3) in rats consuming the higher level of vitamin A. In both groups, vitamin A specific activities in plasma and milk reached apparent plateaus by 2.33 d after addition of [3H]vitamin A to the diets. Vitamin A specific activity in milk was higher than in plasma at all times in both groups. The estimated minimum contribution of chylomicrons to milk vitamin A was 32 +/- 3% in rats fed the lower level of vitamin A vs. 52 +/- 10% at the higher level (P = 0.014). We concluded that dietary vitamin A, like triglycerides, may be directed to mammary tissue during lactation for preferential secretion into milk; thus, increasing vitamin A intakes will increase the contribution of dietary vitamin A to milk. In contrast to milk, mammary tissue vitamin A turns over very slowly.

Animals↗
PubMed2005

Vitamin C and vitamin E for Alzheimer's disease.

OBJECTIVE: To evaluate the literature on supplemental vitamin C and vitamin E therapy in the prevention and treatment of Alzheimer's disease (AD). DATA SOURCES: Literature retrieval was accessed through MEDLINE (1966-March 2005) using the key words antioxidants, vitamin C, vitamin E, Alzheimer's disease, and dementia. International Pharmaceutical Abstracts (1970-March 2005), Current Contents (1996-March 2005), Cochrane Database of Systematic Reviews (1994-March 2005), and Ebsco's Academic Search Elite (1975-March 2005) were searched with the same key words. STUDY SELECTION AND DATA EXTRACTION: Articles related to the objective that were identified through PubMed were included. DATA SYNTHESIS: Oral supplementation of vitamin C (ascorbic acid) and vitamin E (D-alfa-tocopherol acetate) alone and in combination have been shown to decrease oxidative DNA damage in animal studies in vivo, in vitro, and in situ. Recent results of a prospective observational study (n = 4740) suggest that the combined use of vitamin E 400 IU daily and vitamin C 500 mg daily for at least 3 years was associated with the reduction of AD prevalence (OR 0.22; 95% CI 0.05 to 0.60) and incidence (HR 0.36; 95% CI 0.09 to 0.99). Contradicting this is a previous prospective observational study (n = 980) evaluating the relationship between 4 years of vitamin C and E intake and the incidence of AD, which detected no difference in the incidence of AD during the 4-year follow-up. Recent meta-analysis results suggest that doses of vitamin E > or =400 IU daily for more than one year are associated with increased all-cause mortality. Mega-trial results suggest that vitamin E doses > or =400 IU daily for 6.9 years in patients with preexisting vascular disease or diabetes mellitus increase the incidence of heart failure, with no other outcome benefits noted. CONCLUSIONS: In the absence of prospective, randomized, controlled clinical trials documenting benefits that outweigh recently documented morbidity and mortality risks, vitamin E supplements should not be recommended for primary or secondary prevention of AD. Although the risks of taking high doses of vitamin C are lower than those with vitamin E, the lack of consistent efficacy data for vitamin C in preventing or treating AD should discourage its routine use for this purpose.

Alzheimer Disease↗
PubMed2002

Longitudinal concentrations of vitamin B(12) and vitamin B(12)-binding proteins during uncomplicated pregnancy.

BACKGROUND: Because reference values for vitamin B(12) concentrations and vitamin B(12)-binding capacities for pregnant women have not been established, the reference values for nonpregnant women are often applied to assess vitamin B(12) status. The aim of the present study was to describe ranges of biochemical indices of vitamin B(12) status, including red blood cell (RBC) vitamin B(12), saturated and unsaturated cobalamin-binding proteins, and binding capacities in all trimesters of uncomplicated pregnancy. METHODS: A total of 39 healthy pregnant women with long-term daily intake of vitamin B(12) >2.6 microg/day and uncomplicated pregnancies participated in the study throughout their pregnancies. RBCs and serum vitamin B(12), holo-haptocorrin, unsaturated cobalamin-binding proteins, unsaturated and total vitamin B(12)-binding capacities, total homocysteine (tHcy), and RBC count were assessed in weeks 9-12, 20-22, and 36-38 of gestation. RESULTS: Significant changes in vitamin B(12) status occurred in the course of pregnancy. Serum vitamin B(12) concentrations and percentage of saturation of vitamin B(12)-binding proteins decreased steadily throughout pregnancy. In the third trimester, 35% of the participants had serum vitamin B(12) concentrations <150 pmol/L and 68.6% had <15% saturation of total vitamin B(12)-binding capacities, but no women had RBC vitamin B(12) concentrations <148 pmol/L. However, the decrease in these indices was not associated with reduced hemoglobin concentrations or RBC count or with increased tHcy concentrations. CONCLUSIONS: Our findings suggest that the reference values for vitamin B(12) status in nonpregnant women may not be applicable to pregnant women.

Diet↗
PubMedDate not supplied

Vitamin C, vitamin E and cancer (review).

The influences of vitamin C and vitamin E on cancer reported in the literature are reviewed. Several correlational studies and case-control studies suggest that the consumption of vitamin C-containing foods is associated with lower risk for certain cancers, particularly gastric and esophageal cancer. No definite links between dietary vitamin E and human cancer have been demonstrated. Animal and in vitro studies have shown that vitamins C and E can effectively inhibit the formation of carcinogenic nitrosamines. However, animal studies examining the effects of these two vitamins on other chemically-induced cancers are not conclusive. Vitamin C supplementation has been reported to inhibit skin, nerve, lung and kidney carcinogenesis. Vitamin E has been shown to inhibit skin, liver, oral, ear duct, and forestomach carcinogenesis; and to enhance, to have no effect on, or to inhibit mammary gland or colon carcinogenesis, depending upon the method of administration, the level of dietary selenium or fat, and the species and strain of animals used. Both vitamin C and vitamin E can inhibit mutagenesis and carcinogenesis in vitro. Each of the vitamins has been shown to inhibit tumor cell growth and carcinogen-induced DNA damage. The mechanism of action of the two vitamins against carcinogens is not clearly understood. Several suggested mechanisms of action include modification of the metabolism of polycyclic hydrocarbons, reduction of mutagenic activity and reaction with genotoxic free radicals. It is concluded that the potential usefulness of vitamin C and vitamin E in the prevention and treatment of cancer should not be ignored because under certain experimental conditions these two vitamins exert inhibitory effects on chemical carcinogenesis. More carefully standardized and controlled experiments are required to adequately evaluate this potential.

Animals↗
PubMed1999

Comparative effects of vitamin K2 and vitamin E on experimental arteriosclerosis.

The comparative effects of vitamin K2 and vitamin E on aortic calcium (Ca) and inorganic phosphorus (P) levels in the aorta and the elastin fraction (fr.) were investigated in male rats after experimental arteriosclerosis was induced by vitamin D2 with atherogenic diet. Both vitamin K2 (100 mg/kg b.w.) and vitamin E (40 mg/kg b.w.) inhibited the increase of Ca and P in the aorta and the elastin fr. from the arteriosclerotic rats. Vitamin K2 (50 mg/kg b.w.) also suppressed the deposition of Ca and P in the aorta, but there was no change due to vitamin K3 or geranylgeraniol (side chain of vitamin K2) administration. Both vitamin K2 and vitamin E showed lipid radical scavenging activity in the in vitro experiment. However, neither vitamin K3 nor geranylgeraniol exhibited anti-arteriosclerotic or radical scavenging activity under the above experimental conditions. It is suggested that vitamin K2 and vitamin E promoted an antiarteriosclerotic effect by radical scavenging activity. These actions of vitamin K2 are required in the structure of 2-methylnaphtoquinone and its side chain (geranylgeraniol).

Animals↗
PubMed1983

Vitamin fluctuations in the blood of female baboons in relation to normal menstrual cycles, treatments with Lo-Ovral or Depo-Provera and a selected vitamin supplement.

Both endogenous and exogenous sex steriods may induce changes in plasma vitamin levels by altering availability, transport, binding, or use of vitamins. This study investigated some of those mechanisms by observing in a primate model (baboon), the blood levels of carotene, folate, vitamins A, B12, and C, and the status of vitamin B6, riboflavin, and thiamin. The latter three vitamins were studied by determining their relationship to asparate aminotransferase, glutathione reductase, and thiamin transketolase, respectively. The vitamin screen was obtained throughout normal menstrual cycles in 10 baboons and weekly for 55 wk in five baboons receiving Lo-Ovral and in four baboons receiving Provera. During the last 16 wk of hormonal treatment, all baboons received a vitamin supplement containing pyridoxine, riboflavin, and thiamin. Only carotene (p less than 0.0001), vitamin A (p less than 0.05), glutathione reductase (p less than 0.05), and thiamin transketolase (p less than 0.05) levels fluctuated significantly during normal menstrual cycles. Long-term treatment with Lo-Ovral and Provera resulted in numerous changes but there were very few differences between the two hormone treatments. Compared to control levels, vitamin C was elevated during treatment while all three enzyme activities were lowered. Vitamin supplementation raised asparate aminotransferase and glutathione reductase activity and the levels of folic acid, vitamin A, and carotene. This study demonstrates that interactions between hormones and vitamins and among vitamins themselves, are complex but it is likely that the treatments used here caused no physiologically significant vitamin alterations.

Animals↗
PubMed1976

Influence of vitamin B6 intake on the content of the vitamin in human milk.

The influence of the level of vitamin B6 intake on the content of the vitamin in milk was studied in 19 healthy subjects whose stages of lactation ranged from 3 weeks to 30 months. Total vitamin B6 intakes, including extra-dietary sources of the vitamin, ranged from 1.3 to 12.5 mg per day with six subjects consuming less than the recommended allowance of 2.5 mg per day (RDA, 1974). Subjects consuming less than 2.5 mg of vitamin B6 per day had significantly less vitamin B6/liter milk (129 mug) than groups consuming 2.5 to 5.0 or greater than 5.0 mg per day (239 and 314 mug, respectively). Among subjects consuming greater than 2.5 mg of vitamin per day the stage of lactation did not influence the levels of protein or vitamin B6 in milk. Vitamin B6 intakes two to five times the recommended allowance did not significantly elevate the level of the vitamin in milk compared to values for subjects whose intakes approximated the allowance. The vitamin B6/protein ratio in milk of subjects consuming less than 2.5 mg vitamin B6 per day was 13 mug/g and was significantly lower than that observed for the other two groups (23 and 28 mug/g). Daily and weekly variations of the vitamin B6 and protein content in milk of individuals were small. However, marked diurnal variations in the vitamin B6 content were found in milk of individuals taking daily supplements of the vitamin with peak levels occurring in the afternoon 3 to 5 hr after supplements were taken in the morning.

Adult↗
PubMed1997

Changes in vitamin B-6 status indicators of women fed a constant protein diet with varying levels of vitamin B-6.

Changes in vitamin B-6 status indicators were evaluated in vitamin B-6-replete subjects. Ten young women consumed diets providing 85 g protein/d and 1.03, 1.33, 1.73, and 2.39 mg vitamin B-6/d for 12 or 15 d during four successive diet periods; in a second study, six women were fed diets providing 85 g protein/d and 0.84, 1.14, and 2.34 mg vitamin B-6/d for 10 or 12 d during three successive diet periods. Vitamin B-6 status indicators showing significant differences among intakes included urinary excretion of 4-pyridoxic acid and total vitamin B-6, pyridoxal 5'-phosphate and total vitamin B-6 in plasma, and xanthurenic acid excretion after a 2-g L-tryptophan load. Significant correlations were found between vitamin B-6 intake and 4-pyridoxic acid, total vitamin B-6, plasma pyridoxal 5'-phosphate, plasma total vitamin B-6, erythrocyte alanine aminotransferase percentage stimulation and postload excretion of xanthurenic acid and volatile amines (kynurenine plus acetylkynurenine). Depending on the indicator, between 20% and 70% of the subjects had inadequate values for 4-pyridoxic acid, total vitamin B-6, plasma pyridoxal 5'-phosphate, and erythrocyte alanine aminotransferase percentage stimulation at a vitamin B-6 intake of 1.33 mg/d (0.016 mg vitamin B-6/g protein). A ratio of dietary vitamin B-6 to protein > 0.016 mg/g is required for adequate vitamin B-6 status in women.

Adult↗