Liver Concentrations Of Vitamin Research Articles

Vitamin A isotope dilution predicts liver stores in line with long-term vitamin A intake above the current Recommended Dietary Allowance for young adult women

The Estimated Average Requirement (EAR) and Recommended Dietary Allowance (RDA) for vitamin A are 1.7 and 2.4 μmol/d (500 and 700 μg retinol activity equivalents/d), respectively, for nonpregnant, nonlactating women aged >19 y. This intake is presumed to maintain a minimally acceptable liver concentration of 0.07 μmol (20 μg) retinol/g; however, liver reserves have not been evaluated with respect to vitamin A intake in women of any age group defined in the Dietary Reference Intakes. This cross-sectional study examined vitamin A intake and liver reserves estimated by stable-isotope dilution testing. Forty nonpregnant, nonlactating women (mean ± SD age: 22.4 ± 2.3 y) completed a Harvard food-frequency questionnaire (FFQ) and 3-d diet record (3DDR) before undergoing vitamin A status assessment by using a [(13)C2]retinol stable-isotope dilution test. Vitamin A intake was 70% higher than the RDA by both dietary-assessment methods (P < 0.001). The mean (±SD) liver concentration of vitamin A was 0.45 ± 0.31 μmol/g (129 ± 89 μg/g) and ranged from 0.09 (26 μg/g) to 1.79 μmol/g (513 μg/g). Liver and total-body vitamin A were highly correlated with intake measured by FFQ (P ≤ 0.009), but 3DDR was not (P ≥ 0.22). Prediction equations were developed for 3- and 7-d data. In this well-nourished population, vitamin A consumption was considerably higher than recommended, and liver reserves were consistent with intake. Because of their sensitivity, stable-isotope techniques can help to describe the vitamin A status and better characterize the intake needs of all groups defined in the Dietary Reference Intakes. Registration was not required for this trial.

Urinary Excretion of Water-Soluble Vitamins Increases in Streptozotocin-Induced Diabetic Rats without Decreases in Liver or Blood Vitamin Content

It is thought that the contents of water-soluble vitamins in the body are generally low in diabetic patients because large amounts of vitamins are excreted into urine. However, this hypothesis has not been confirmed. To investigate this hypothesis, diabetes was induced in male Wistar rats (6 wk old) by streptozotocin treatment, and they were then given diets containing low, medium or sufficient vitamins for 70 d. The contents of 6 kinds of B-group vitamins, namely vitamin B₁, vitamin B₂, vitamin B₆, vitamin B₁₂, folate and biotin, were determined in the urine, blood and liver. No basic differences among the dietary vitamin contents were observed. The urinary excretion of vitamins was higher in diabetic rats than in control rats. The blood concentrations of vitamin B₁₂ and folate were lowered by diabetes, while, those of vitamin B₁, vitamin B₂, vitamin B₆, and biotin were not. All liver concentrations of vitamins were increased in diabetic rats above those in control rats. These results showed that streptozotocin-induced diabetes increased urinary excretion of water-soluble vitamins, though their blood and liver concentrations were essentially maintained in the rats.

The Effect of Carrier for Vitamin E on Liver Concentrations of Vitamin E and Vitamin E Excretion in Broilers ,

Two experiments were conducted to determine the effect of 2 carrier sources of vitamin E on growth performance and excreta and liver vitamin E concentrations of broilers. Chicks were pretested from d 0 to 7 posthatching on a corn-soybean meal diet without vitamin E supplementation, and the experiments lasted from d 7 to 19 posthatching. Each treatment in both experiments was replicated with 6 pens with 5 chicks each. Initial and final BW were 155 and 684 g in experiment 1 and 155 and 691 g in experiment 2. In experiment 1, the dietary treatments were the corn-soybean meal diet with varying concentrations (0, 30, 100, or 300 IU/kg) of supplemental vitamin E either absorbed to verxite (VE) or adsorbed to silica (SE). In experiment 2, the dietary treatments were the 0 and 30 IU/kg of vitamin E as VE or SE. In experiment 1, feed intake decreased and gain:feed increased as concentration of VE increased, but feed intake increased and gain:feed decreased as concentration of SE increased (source x concentration, P < 0.03). Gain, feed intake, and gain:feed were not affected (P > 0.10) by the vitamin E carrier source in experiment 2. The mean excreta vitamin E concentration at d 7 posthatching was 17.2 IU/kg (DM basis). The percentages of vitamin E excreted were based on analyzed vitamin E concentrations in the diet. At 100 and 300 IU/kg of supplemental vitamin E, an average of 94 and 44% of vitamin E intake from broilers fed vitamin E from VE and SE, respectively, was excreted (vitamin E source, P < 0.01; source x concentration, P < 0.08), but at 30 IU/kg of vitamin E, 49 and 45% of vitamin E intake from broilers fed vitamin E from VE and SE was excreted. In experiment 2, 52 and 43% of vitamin E intake from VE and SE was excreted (source, P < 0.02). Liver alpha-tocopherol concentration was not different (P > 0.10) between the sources of vitamin E in either experiment. Increased concentrations of vitamin E increased liver alpha-tocopherol concentrations (P < 0.01). On the basis of the results of excreted vitamin E, vitamin E adsorbed to SE was more available than vitamin E absorbed to VE, but on the basis of liver vitamin E concentration, their availabilities were similar.

Effect of selenium and Ascaridia galli infection on antioxidant biomarkers in broiler chickens: a mathematical model for parasite reduction and host growth

The activity of selenium-dependent glutathione peroxidase (GPX), liver concentration of vitamin E, and plasma and liver selenium levels were used for estimation of the antioxidant status of broiler chickens infected with Ascaridia galli. These biomarkers were recorded in an experiment covering 70 days p.i. At the same time the establishment rate of A. galli in chicken intestines, gain in the host body weight and chicken survival were studied. Broiler chickens (Cobb hybrids) were infected with 1450 embryonated A. galli eggs and treated with Sel-plex. A mathematical model was applied to determine the rate of nematode reduction and the relative rate of gain of host body weight, which are essential kinetic parameters of parasite-host interaction. The activity of GPX increased with both elevated selenium and reduced infection levels. The concentrations of selenium and vitamin E, and the GPX activity in the infected chickens demonstrated a similar pattern of change with time after day 30 p.i. The supplementation of the broilers with dietary selenium in the form of Sel-plex improved their antioxidant status. Increases by 29% in vitamin E concentration, 15% in GPX activity, and 22% in liver selenium concentration, respectively, were recorded in the infected and treated, compared to infected and untreated broilers.

Hepatic and renal concentrations of vitamins E and C in lead- and ethanol-exposed rats. An assessment of their involvement in the mechanisms of peroxidative damage

The study was aimed at investigating vitamin E and vitamin C concentrations in a liver and kidney as well as their involvement in the mechanism of peroxidative action of lead (Pb) and ethanol (EtOH) in these organs in rats receiving 500 mg Pb/l (in drinking water) or/and 5 g EtOH/kg body wt./24 h (p.o.) for 12 weeks. The exposure to Pb and EtOH alone and in combination led to a decrease in vitamin E concentration in the liver compared to the control group (by 30%, 26% and 50%, respectively). The decrease in the liver vitamin E concentration in the rats co-exposed to Pb and EtOH was more marked than in those separately treated with these xenobiotics. The treatment with Pb alone and in combination with EtOH led to a decrease in vitamin E concentration in the kidney (by 13% and 21%, respectively). The liver vitamin C concentration decreased as a result of exposure to EtOH, both separately (by 17%) and in combination with Pb (by 11%). The kidney vitamin C concentration increased in the rats exposed to EtOH alone (by 10%), whereas in those treated with Pb, both separately and in combination with EtOH it decreased (by 26% and 6%, respectively). ANOVA/MANOVA analysis revealed that the changes in vitamin E concentration in the liver and kidney at co-exposure to Pb and EtOH resulted from their independent action, whereas those in vitamin C were due to an independent action of these xenobiotics (EtOH in the liver, Pb and EtOH in the kidney) and an interaction between them. There was no correlation between vitamins E and C concentrations in the liver and kidney. The liver concentration of vitamin E and the liver and kidney concentration of vitamin C negatively correlated with malondialdehyde concentration (MDA, lipid peroxidation index) in these organs. Based on the results of the present study and our previous findings in this experimental rat model it can be hypothesized that vitamins E and C are involved in the mechanism of peroxidative action of Pb and EtOH in the liver and kidney, both at separate and combined exposure. The probable protective involvement of vitamins E and C in the damaging action of EtOH and Pb may be related to scavenging of free radicals directly and indirectly generated by these xenobiotics.

Vitamin and thyroid status in arctic grayling ( Thymallus arcticus) exposed to doses of 3,3 ′,4,4 ′-tetrachlorobiphenyl that induce the phase I enzyme system

Induction of phase I biotransformation enzymes is recognized as a hallmark response in fish exposed to coplanar PCBs. Depletions of vitamins A and E and disrupted thyroid hormone and glandular structure secondary to this induction have not yet been examined in an arctic fish species. Arctic grayling were exposed to a single oral dose of 0 (control), 10, 100 or 1000 ng 3,3 ′,4,4 ′-tetrachlorobiphenyl (TCB) g −1 bodyweight, a contaminant found in most arctic fish. After 30 and 90 days of exposure, TCB concentrations in tissues, hepatic phase I activity (as ethoxyresorufin-O-deethylase (EROD)), plasma and tissue vitamin A and E concentrations, plasma thyroid hormone levels and thyroid glandular structure were examined. Total plasma osmolality, as an indicator of overall fish health was also monitored. TCB recovery in tissues was low and extremely variable, making comparisons between intended dose groups inappropriate. Therefore, correlation analysis between actual recovered TCB concentrations and biochemical responses was employed. Hepatic EROD activity correlated strongly with liver TCB concentrations. Liver concentrations of vitamin A were altered as a function of TCB concentrations and EROD activity, but plasma vitamin A status was not affected. Vitamin E was depleted by TCB accumulation in blood and EROD induction in liver of males only at 90 days post-exposure. Thyroid hormones status and glandular structure were not affected by the short duration TCB exposures used in this experiment. TCB concentrations were correlated with an elevation in plasma osmolality. Results from this experiment indicate that the vitamin status and osmoregulation of arctic grayling exposed to TCB can be compromised. Further studies of field populations exposed to this type of contaminant are warranted.

Absence of adverse effects of sodium metabisulphite in manufactured biscuits: results of subacute (28-days) and subchronic (85-days) feeding studies in rats

Sulphites are extensively used in the food and drinks industry. Their toxicity has been previously evaluated by addition to the diet or drinking water of laboratory animals. Because interactions between sulphites and food constituents occur, the present work was conducted to determine the subacute and subchronic toxicity of sulphite-bound compounds in a finished product: manufactured biscuits. The studies were performed on Sprague Dawley rats for 28 and 85 days of dietary exposure. Diets were prepared from sulphited or untreated (controls) biscuits with the addition of sugar, protein, vitamins and minerals according to the nutritional requirements of the animals. Groups of 10 male and 10 female rats were administered diets containing sulphited biscuits at levels of 0, 10, 35 and 75%, corresponding to 10–15, 35–45, 150–170 and 310–340mg SO2/kg diet. In both studies, no death or clinical abnormalities were reported. Growth rate, food consumption and food conversion efficiency were not affected by treatment. No dose-related changes were observed for haematology, clinical chemistry, ocular examination, renal-function, urinalysis, organ weights or gross and microscopic examinations. The liver concentrations of vitamins A, B1, C and E were not significantly changed except for an increase in vitamin E in high-dose males after 28 days' exposure. Based on these data, the no-observed-adverse-effect level (NOAEL) of sulphites in baked biscuits was judged to be 310mg SO2/kg diet or 25mg/kg body weight/day.

Vitamin B-12 Deficiency and Hyperhomocysteinemia Are Partly Ameliorated by Cobalt and Nickel Supplementation in Pigs

Vitamin B-12 deficiency and hyperhomocysteinemia alter the metabolism of trace elements. This study tested the hypothesis that there is a reverse relationship in which diets high in iron, copper, nickel and cobalt would influence vitamin B-12 deficiency outcomes including hyperhomocysteinemia. Piglets (German Landrace x Pietrain) were assigned to six groups of 8 and fed one of the following diets for 166 d: a vitamin B-12-adequate and folate-fortified diet (30 microg/kg vitamin B-12 and 0.5 mg/kg folate) with normal trace element concentrations or one of five vitamin B-12-free, folate nonsupplemented diets (0.36 mg/kg), with either normal trace element concentrations or high concentrations of iron (300 mg/kg), copper (30 mg/kg), cobalt (1 mg/kg) or nickel (6 mg/kg). Feed intake and weight gain did not differ significantly among the groups. Vitamin B-12-deficient pigs developed diminished serum and liver concentrations of vitamin B-12 and folate, an accumulation of iron in the liver and hyperhomocysteinemia. The magnitude of changes differed among vitamin B-12-deficient groups. Vitamin B-12-deficient pigs fed 6 mg/kg nickel had distinctly higher vitamin B-12 concentrations in liver and serum and 45% lower serum concentration of homocysteine than the corresponding deficiency group fed 1 mg/kg nickel; iron concentration in liver was completely normalized. Vitamin B-12-deficient pigs fed 1 mg/kg cobalt had 47% lower homocysteine concentrations in serum than the vitamin B-12-deficient group fed 0.13 mg/kg cobalt, but the vitamin B-12 status was unaffected. Supplementation of iron and copper did not affect these variables. The dietary manipulations had no detrimental effects on variables symptomatic of oxidative stress. The findings indicate a collaborative relationship between vitamin B-12 metabolism and the trace elements nickel and cobalt.

Use of the Relative Dose Response (RDR) Assay to Determine Vitamin A Status of Calves at Birth and Four Weeks of Age1,2

An accurate assessment of vitamin A status can be determined by analysis of liver biopsy samples; however, liver biopsies are not always feasible. Plasma concentrations of vitamin A do not provide an accurate indication of vitamin A status. The objective of this study, therefore, was to determine the ability of the relative dose response assay to indicate the vitamin A status of Holstein calves. Calves were obtained at birth and assigned to vitamin A treatments (0, 1700, 34,000, or 68,000 IU/d) added to milk replacer. Liver biopsies and relative dose response assays were per-formed at birth and 4 wk. Calves supplemented with 1700, 34,000, or 68,000 IU of vitamin A/d had adequate (greater than 20µg/g) liver concentrations of vitamin A at 4 wk of age. The relative dose response assay at 4 wk was correlated with liver concentrations of vitamin A. Both the relative dose response assay and liver concentrations of vitamin A indicated that calves not supplemented with vitamin A had low vitamin A status, whereas other treatment groups had adequate vitamin A status. Plasma concentrations of retinol increased theby 4 wk of age in calves receiving supplemental vitamin A at 34,000 IU and 68,000 IU/d and decreased in unsupplemented calves; however, all calves had concentrations of <20μg of retinol/dl of plasma. The relative dose response assay agreed with liver biopsies as an indication of vitamin A status, whereas plasma concentrations of retinol incorrectly indicated all treatment groups were deficient in vitamin A.

Evaluation of oxidative stress based on lipid hydroperoxide, vitamin C and vitamin E during apoptosis and necrosis caused by thioacetamide in rat liver

After 12 h of thioacetamide (500 mg/kg body weight) administration to rats, the activity of caspase-3-like protease in the liver increased significantly compared to that in the control group. In plasma, the activity of caspase-3 was barely detectable in the control rat, but had increased significantly after 24 h of drug administration along with a dramatic increase in GOT. These results indicate that thioacetamide causes apoptosis in the liver by activating caspase-3, which is released to plasma by successive necrosis. At 24 h, the concentration of liver lipid hydroperoxides, a mediator of radical reaction, was 2.2 times as high as that of control rats. After 12 and 24 h of thioacetamide administration, the liver concentrations of vitamins C and E decreased significantly. The decrease of antioxidants and formation of lipid hydroperoxides 24 h after thioacetamide administration support the view that extensive radical reactions occur in the liver during the necrotic process.

In Well-Fed Young Rats, Lactose-Induced Chronic Diarrhea Reduces the Apparent Absorption of Vitamins A and E and Affects Preferentially Vitamin E Status

To establish the effect of lactose-induced diarrhea on the apparent absorption and status of vitamins-A and E in well-fed young rats, we fed Sprague Dawley rats a balanced diet or a lactose diet (350 g/kg). A group of rats fed the control diet equal to the level measured in the lactose-fed rats (pair-fed) was also included. The experiment lasted 23 d and feces were collected on days 4–6, 10–12, 14–16 and 20–22. Samples of serum and tissues were taken on days 10 and 23. Lactose caused a significant reduction in food intake, had no effect on body weight and produced a diarrhea that persisted during the whole experiment. The severity of diarrhea decreased with time, indicating that the rats partially adapted to lactose feeding. At the onset of diarrhea, the apparent absorption of vitamins A and E in the rats with diarrhea was significantly lower than in the control or pair-fed rats, but the rats with diarrhea recovered gradually, and in the case of vitamin E was normalized by day 15. At day 10 the rats with lactose-induced diarrhea had serum and liver concentrations of vitamins A and E that did not differ from the control or pair-fed rats. However, at day 23 the lactose-fed rats with diarrhea had significantly lower serum and liver concentrations of vitamin E than the control or pair-fed rats. Measured at that time, diarrhea had no effect on liver vitamin A, but lower serum concentrations of this vitamin were detected in both the lactose-fed rats and in the pair-fed rats. In general, in well-nourished rats, the chronic diarrhea associated with excessive dietary lactose reduced the apparent absorption of vitamin A and E and particularly compromised the nutritional status of vitamin E.

Olestra's Effect on the Status of Vitamins A, D and E in the Pig Can Be Offset by Increasing Dietary Levels of These Vitamins , ,

Groups of weanling pigs (5 castrated males, 5 females per group) were fed purified diets containing the NRC's requirements for nutrients and 0, 1.1, 4.4 or 7.7% olestra for 12 wk. Graded concentrations of vitamins A, D2 and E were added at each olestra concentration. The primary purpose of the study was to establish relationships between dietary concentration of olestra and the amounts of vitamins A, D2 and E needed to restore tissue concentrations of these vitamins to control concentrations. A secondary purpose was to confirm that olestra does not affect the status of vitamin K or water-soluble nutrients. Liver concentrations of vitamins A, E and B12, iron and zinc and bone concentrations of ash, zinc, calcium and phosphorus, were measured in a group of pigs killed at the start of the study and in all pigs killed at wk 12. Growth, feed efficiency, hematology, clinical chemistry, blood concentrations of retinol, α-tocopherol, 25-hydroxyergocalciferol, 25-hydroxycholecalciferol, 1,25-dihydroxyvitamin D, folate, iron, total iron-binding capacity, zinc and calcium and adipose concentration of vitamin E were measured at 4-wk intervals. Prothrombin time was measured weekly for the control and 7.7% olestra groups, monthly for others. Relationships derived from measured tissue concentrations of vitamins A and E showed that constant amounts of the vitamins were required per unit mass of olestra in the diet to restore tissue concentrations to control values. Such a relationship could not be determined for vitamin D because exposure of the pigs to UV light resulted in an apparent interaction between vitamin D2 and vitamin D3. Olestra did not affect growth, digestible feed efficiency, vitamin K status or the status of the water-soluble micronutrients, in agreement with other studies in the pig.

Nutritional Status of Pigs Fed Olestra with and without Increased Dietary Levels of Vitamins A and E in Long-Term Studies , ,

In a 26-wk study, five groups (n = 10) of domestic pigs were fed 0.25, 0.5, 1.1, 3.3 or 5.5% olestra; three groups were fed 0.25% with graded levels of vitamins A and E; and one group was fed 5.5% with added vitamins A and E and exposed to UV light. In a 39-wk study, two groups (n = 10) were fed 0.25% olestra with or without added vitamins A and E. In each study, a control group was fed basal diet with no olestra, and a group was killed at d 0 for base-line nutrient measurements. The diets provided the NRC's requirements of micronutrients for 5- to 10-kg pigs, with the following two exceptions: vitamin D was provided at twice the requirement in the 26-wk study and vitamin K was provided at 20% of the requirement in the 39-wk study. One purpose of the studies was to determine the amounts of vitamins A and E required to restore tissue concentrations of those vitamins to control concentrations. A second purpose was to determine the effects of olestra on the status of vitamins A, D, E, K and B12, and folate, iron, calcium and zinc when pigs eat olestra at intakes similar to estimated human intake for a period covering major growth and developmental phases, including sexual maturation. Olestra reduced tissue concentrations of vitamins A, D and E but did not affect prothrombin time or the status of the water-soluble nutrients. The amount of vitamin A required to restore liver concentration to control concentration was 93 μg retinyl palmitate/g olestra. Restoration levels for serum and liver concentrations of vitamin E were 2.2 and 2.1 mg d-α-tocopheryl acetate/g olestra. Olestra did not affect growth or digestible feed efficiency in either study, indicating that the absorption and utilization of macronutrients were unaffected. There were no antemortem observations or changes in clinical chemistry or hematology that would indicate an adverse effect of olestra.

Plasma and tissue concentrations of vitamin E following supplementation of two forms of vitamin E in sheep

Twenty-five lambs were used to determine the plasma and tissue concentrations of vitamin E after oral supplementation of two forms and in two doses. Five lambs were assigned to each of the following treatments: (1) control, no supplemental vitamin E, (2) 500 IU of DL-α-tocopherol, (3) 500 IU of D-α-tocopherol, (4) 1000 IU of DL-α-tocopherol, and (5) 1000 IU of D-α-tocopherol. Animals were supplemented daily with either 500 or 1000 IU of their respective vitamin E sources for 28 consecutive days. Blood samples were collected twice a week until Day 28. Animals were subsequently slaughtered at Day 28 and ten different tissues were collected for α-tocopherol analysis. All supplemented groups were higher in plasma α-tocopherol concentration than the control. When sheep were dosed with 500 IU there was a tendency for higher plasma concentration following D-α-tocopherol than DL-α-tocopherol administration and this difference became significant after 1000 IU dosing ( P < 0.05). Tissue α-tocopherol concentrations for all treatment groups were higher than those of control. Across all treatments, the highest α-tocopherol concentrations were noted in liver and pancreas and the lowest in neck and hip muscle. Results of this study suggested that in lambs blood and liver concentrations of vitamin E were higher following supplementation of D-α-tocopherol than with DL-α-tocopherol. Supplementation of vitamin E resulted in accumulation of different levels of α-tocopherol in different organs.

Effect of Insulin Treatment or Zinc Supplementation on Vitamin A Status in Streptozotocin-Induced Diabetic Rats.

A Using streptozotocin-induced diabetic rats, we examined the effects of zinc supplementation and insulin treatment on the metabolic availability of vitamin A. All diabetic animals exhibited an elevated plasma glucose (>18 mmol/liter) level within 48 h of intravenous streptozotocin injection. The untreated diabetic rats exhibited a reduction in body weight gain, with a 50% increase in daily food intake. In diabetic animals treated with insulin for 4 weeks, the plasma glucose, body weight gain, and daily food intake were comparable to those of the non-diabetic controls. The plasma concentration of vitamin A was significantly reduced in the diabetic animals, whereas the hepatic content of vitamin A in them was significantly elevated. Treatment with implantable insulin resulted in both plasma and liver concentrations of vitamin A returning to the control non-diabetic levels. Dietary zinc supplementation (120 µg/g diet for 4 weeks) failed to improve the plasma concentration of vitamin A. These results suggest that the impaired metabolic availability of vitamin A in the presence of diabetes is caused by insulin deficiency.

Serum and liver concentrations of vitamin K in surgical patients.

Serum and liver concentrations of vitamin K in surgical patients.

Vitamin E inhibition of lipid peroxidation and ethanol-mediated promotion of esophageal tumorigenesis.

Promotion of chemically induced esophageal cancer by ethanol may include the generation of highly reactive free radicals and thus may be preventable by the antioxidant vitamin E. In the present study, female C57BL/6 mice received N-nitrosomethylbenzylamine (NMBzA, 0.2 mg/kg ig) three times a week for three weeks. After this esophageal carcinogenic treatment, mice were fed a nutritionally adequate liquid diet with 30% of the calories supplied by ethanol or an isocaloric carbohydrate with or without supplemental alpha-tocopherol (142 mg/kg diet). As a marker of in vivo lipid peroxidation, exhaled ethane was collected and measured 24 hours "before" the mice were killed after 20 weeks of dietary treatment. Hepatic malondialdehyde, lipid fluorescence, and conjugated dienes were determined as markers of products of lipid peroxidation and serum aminotransferases as indexes of liver toxicity. Hepatic liver concentrations of vitamins A and E and the size and frequency of esophageal tumors were also assessed. Ethanol consumption after NMBzA administration significantly increased (p less than 0.05) the size and frequency of esophageal tumors. These ethanol-promoted effects were accompanied by increases in indexes of in vivo and accumulated products of lipid peroxidation. Similarly treated animals that received supplemental dietary vitamin E showed significant reductions (p less than 0.05) in mean tumor size and frequency of tumors as well as a decrease in the indexes of hepatic lipid peroxidation. The results suggest that promotion of NMBzA-induced esophageal tumors by ethanol may in part result from increased lipid peroxidation and that vitamin E reduces carcinogenicity of NMBzA or ethanol promoter effects by inhibiting lipid peroxidation.

Hypertension portale et hypervitaminose A. À propos de deux cas et Revue de la littérature

Portal hypertension consecutive to hypervitaminosis A has seldom been well documented. Two cases are reported here. The first case concerns a 39-year old woman who had taken meladinine (8-methoxypsoralen) for the purpose of tanning. In the second case, a 43-year old woman had absorbed Plethoryl (a combination of tiratricol, cyclovalone and retinol) in order to lose weight. Both patients had histological hepatic lesions, such as hypertrophic Ito cells, perisinusoidal cirrhosis and spontaneous autofluorescence, suggestive of vitamin A overload, associated with a hepatic vein pressure gradient of 10 mmHg or more and high liver concentrations of vitamin A. The responsibility of Plethoryl in case 2 is beyond any doubt, but the mechanism of hypervitaminosis in case 1 is controverted. A review of the literature has provided detailed information on the signs of vitamin A overload, the frequency of which is probably underestimated. Patients with portal hypertension of unknown origin should be investigated for hypervitaminosis A.

Retinol Storage in the Rat Liver after Daily Intramuscular Administration of Physiological Doses of a Vitamin A Oil Emulsion

We have recently shown the kinetic behavior of liver retinyl esters in rats with adequate vitamin A levels receiving oral vitamin supplementation. In the present work we have studied the effects of intramuscular administration of a vitamin A preparation on the metabolism of vitamin A in the rat. Retinol administered intramuscularly to rats in the form of an emulsion brought about a significant increase in the serum and liver concentration of vitamin A; this increase was slightly less than in orally treated rats. In each group, retinyl palmitate constituted 80-85% of the total retinyl esters, followed by stearate (9-13%), laurate, palmitoleate, myristate, linoleate and pentadecanoate making up 3-10%. The subcellular localization of all retinyl esters is similar and dependent on age but not on the route of administration. These results indicate that although the best hepatic storage is achieved with an orally administered vitamin A emulsion, the intramuscular administration of a physiological dose might provide an effective supplementation method if oral vitamin A is contraindicated.

Megadose Effects of Vitamin C on Vitamin B-12 Status in the Rat

Effects of ascorbic acid ingestion on the severity of vitamin B-12 deficiency were investigated by feeding weanling rats experimental diets containing 0-100 micrograms of vitamin B-12 activity per kg of diet, with or without 6.0 mg of ascorbic acid per ml supplied in drinking water for 15 wk. This daily consumption of up to 150 mg of ascorbic acid did not impair growth, but did result in significantly higher concentrations of ascorbic acid in plasma, liver, adrenal glands and feces. When rats were fed diets deficient or marginally deficient in vitamin B-12, liver concentrations of vitamin B-12 were markedly lower than in liver of rats fed adequate vitamin B-12. Ascorbic acid ingestion raised values significantly in the vitamin B-12-deficient diet group. Urinary methylmalonic acid was significantly elevated in the deficient rats. However, it was significantly reduced to more normal values by ascorbic acid in rats with both low and marginal vitamin B-12 status, as defined by dietary and liver concentrations of vitamin B-12 activity. Although coprophagy was not prevented, rats showed no increased consumption of feces with the higher ascorbic acid content. Thus, the results of this research indicate that vitamin C ingestion partially protects rats from vitamin B-12 deficiency.