Effects of supplemental vitamin A on retinoic acid concentrations in the plasma of preruminant calves

Neonatal calves are fed frequently milk replacers with vitamin A concentrations exceeding those recommended by the National Research Council. The vitamin A metabolite, retinoic acid (RA), affects profoundly cellular differentiation and homeostasis. For this reason, effects of dietary vitamin A on plasma concentrations of RA isomers in milk replacer-fed calves were examined. Male, Holstein calves (n = 24) were fed colostrum within 12 hours after birth and, thereafter, a custom-formulated low vitamin A milk replacer providing 0, 1700 [National Research Council (NRC) daily requirement for young growing calves] (controls), 34,000 (industry standard in the United States) or 68,000 IU of vitamin A daily. Concentrations of retinol and RA isomers in plasma samples collected from birth to 27 days of age were determined by HPLC. Retinol was affected by dietary vitamin A with higher concentrations occurring in calves supplemented with > or = 34,000 IU of vitamin A/day than in control (1700 IU of vitamin daily) and unsupplemented calves. Relative to controls, concentrations of all isomers of RA were higher in calves supplemented with > or = 34,000 of vitamin A daily during the experimental period. The predominant isomer in all calves was 9,13-dicis-RA. In control calves, 9,13-dicis-RA and 9-cis-RA were maximal at 1 to 6 days of age and then decreased progressively. In calves fed > or = 34,000 IU of vitamin A daily, concentrations of these isomers were markedly higher at 6 days of age, relative to controls, and remained elevated for the duration of the study. In all calves, retinol was correlated positively with 9,13-dicis- and 9-cis-RA from 9 to 27 days of age. 9,13-cis-Retinoic acid was correlated positively with 9-cis- and 13-cis-RA from 13 to 27 days of age. It is concluded that supplementing milk replacer-fed calves with vitamin A at levels exceeding current NRC recommendations by > or = 20-fold causes an elevation in plasma concentrations of retinol and retinoic acids. 9,13-dicis- and 9-cis-Retinoic acids were most affected by supplemental vitamin A. Physiologic consequences of increased plasma RA concentrations induced by high dietary levels of vitamin A warrant investigation.     

Estimation of the dietary vitamin A requirement of juvenile grass shrimp, Penaeus monodon

Two growth experiments were conducted to estimate the minimal dietary vitamin A requirement for juvenile grass shrimp, Penaeus monodon. In expt. 1, purified diets containing 0, 1,500, 3,000, 15, 000, 30,000, 45,000 and 60,000 retinol equivalent (RE)/kg (i.e., 0, 5,000, 10,000, 50,000, 100,000, 150,000, 200,000 IU/kg) of supplemental vitamin A (retinyl acetate) were fed to P. monodon (mean initial weight 0.97 +/- 0.01 g) for 8 wk. In expt. 2, diets with 0, 600, 1,200, 1,800, 2,400, 3,000, 3,600, and 4,500 RE/kg (i.e. , 0, 2,000, 4,000, 6,000, 8,000, 10,000, 12,000, 15,000 IU/kg) of supplemental vitamin A were fed to the shrimp (mean weight 0.68 +/- 0.01 g) for 6 wk. The basal unsupplemented diet contained 54 RE vitamin A/kg, and supplemental levels were confirmed by analysis. Each diet was fed to three replicate groups of shrimp. In expt. 1, shrimp fed diets supplemented with 300 RE vitamin A/kg had significantly greater weight gain (P < 0.05) than those fed the unsupplemented control diet and diets supplemented with >===" BORDER="0">30,000 RE vitamin A/kg. Survival rate was higher in shrimp fed diets supplemented with 1,500-30,000 RE vitamin A/kg than shrimp fed the control diet. Highest blood triglyceride concentration and body lipid concentration were in shrimp fed diets supplemented with 45,000 and 60,000 RE vitamin A/kg, respectively. Eye vitamin A concentration and hepatopancreatic total lipid concentration in shrimp generally increased as dietary vitamin A supplementation increased. In expt. 2, feed efficiency was highest in shrimp fed diets supplemented with 2,400, 3,000, 3,600 and 4,500 RE vitamin A/kg, followed by shrimp fed diets with 600 and 1,200 RE vitamin A/kg and finally the unsupplemented control group. Shrimp fed diets supplemented with vitamin A had significantly higher survival percentages than those fed the unsupplemented control diet. Weight gain percentage of the shrimp analyzed by broken-line regression indicated that the minimal dietary vitamin A concentration in growing P. monodon is 2,511 RE/kg ( approximately 8, 400 IU/kg).     

Effects of dietary vitamin E and high supplementation of vitamin C on plasma glucose and cholesterol levels

Weanling male Sprague Dawley rats were fed ad libitum a purified basal diet free of vitamins E and C. In Experiment I (4 weeks), 24 rats were divided into four groups with 2×2 factorial design. They were supplemented with 0 or 45 IU/kg diet of vitamin E, and O or 2.0 g/kg diet of vitamin C. In Experiment II (16 weeks), 36 rats were divided into six groups with 2×3 factorial design. Vitamin E was supplemented at the level of O or 45 IU/kg diet, and vitamin C was supplemented at the level of O, 1.5, or 3.0 g/kg diet, respectively. Plasma glucose level and cholesterol level were determined in both experiments. The plasma levels of glucose and cholesterol were significantly and negatively correlated. Plasma glucose level was significantly increased and plasma cholesterol level significantly decreased by the high supplementation of vitamin C with or without vitamin E in the diet. Vitamin E deficiency decreased plasma glucose level and increased plasma cholesterol level significantly with or without vitamin C supplementation. The groups with adequate level of vitamin E (45 IU/kg diet) and no vitamin C showed moderate plasma glucose and cholesterol levels.     

Concentration of plasma and milk vitamin E and plasma beta-carotene of mastitic and healthy cows.

Variation of vitamin E in blood plasma and milk and beta-carotene in blood plasma of 38 healthy and 38 mastitic cows was studied. Cows were assigned to one of the two treatment groups: control and vitamin E supplemented. Vitamin E supplementation was started when cows were dried-off at the end of lactation and continued until 3 months post partum at the rate of 1000 IU per cow daily and then reduced to 500 IU for the remaining lactation. A cow was considered mastitic when somatic cell count of milk was greater than 500 x 10(3) cells/ml. Milk samples with somatic cell counts below 100 x 10(3) cells/ml were from healthy cows. Data on vitamin E concentration of plasma and milk and beta-carotene in plasma were analyzed by a least squares procedure. The model included the effects of treatment, mastitis status, stage of lactation, and all first order interactions. Mean vitamin E levels in plasma and milk of supplemented cows were significantly higher than of the non-supplemented cows. Plasma and milk levels of vitamin E as well as beta-carotene in plasma were significantly lower in mastitic than healthy cows. When data were analyzed with loge, of somatic cell count in milk as an independent regression variable, results were similar. There was a negative correlation of mastitis status with vitamin E levels in plasma (-0.48), milk (-0.24), and beta-carotene in plasma (-0.38).(ABSTRACT TRUNCATED AT 250 WORDS)     

25-Hydroxyvitamin D and vitamin D in human milk: effects of supplementation and season

Breast-milk 25-hydroxyvitamin D (25-[OH]D) and vitamin D were measured in mothers supplemented with 2000 or 1000 IU (50 or 25 micrograms) of vitamin D/d or with no supplementation. Fore- and hindmilk samples were collected at two stages of lactation (8 and 15 or 20 wk after delivery) and at different seasons. Season affected the levels of 25-(OH)D and vitamin D. The 25-(OH)D levels were higher in hind- than in foremilk. Supplementation had no effect on vitamin D levels. Milk 25-(OH)D levels of mothers receiving either 1000 or 2000 IU (25 or 50 micrograms) vitamin D/d were significantly higher than those of unsupplemented mothers in February and April. In theory, supplementation with 2000 IU (50 micrograms) vitamin D should have increased the calculated antirachitic activity of the milk in winter to the levels of unsupplemented mothers in September; however, responses varied widely among individuals.     

The effect of vitamin E (alpha-tocopherol) supplementation on hepatic levels of vitamin A and E in ethanol and cod liver oil fed rats

Eight groups of 5 rats were fed 8 differing liquid diets with and without ethanol, cod liver oil and/or increased levels of vitamin E. Hepatic levels of vitamins A and E were determined following the 28-day feeding time. Ethanol consumption decreased the levels of hepatic vitamin E (p less than 0.05), vitamin A (p less than 0.05) and the ratio of vitamin A/E (p less than 0.05). Hepatic levels of vitamins A and E were unaffected in rats fed cod liver oil. Supplementation of the normal dietary level of 30 IU of vitamin E per kg diet, with an additional 142 IU alpha tocopherol/kg diet, restored hepatic concentrations of vitamin E to normal levels in alcohol-fed rats. The hepatic levels of vitamin A in rats fed ethanol diets supplemented with vitamin E were less than that of control rats but were 4.3 times greater than that of rats on ethanol diets unsupplemented with vitamin E. However, the vitamin A and E ratio was equal to normal in this group of rats. The vitamin A/E ratio was reduced in liver of rats fed non-alcoholic diets supplemented with vitamin E due to increased levels of hepatic vitamin E. Additionally, rats fed cod liver oil diets containing ethanol also indicated decreased hepatic vitamin A and E levels. However, these levels were greater than that of rats fed only alcoholic diets suggesting that these vitamins are replaced by the vitamin A and E content in the cod liver oil.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hepatic vitamin A preloading reduces colorectal cancer metastatic multiplicity in a mouse xenograft model

Previous research in our laboratory showed that retinol inhibited all-trans retinoic acid (ATRA)-resistant human colon cancer cell invasion via a retinoic acid receptor-independent mechanism in vitro. The objective of the current study was to determine if dietary vitamin A supplementation inhibited metastasis of ATRA-resistant colon cancer cells in a nude mouse xenograft model. Female nude mice (BALB/cAnNCr-nu/nu, n = 14 per group) consumed a control diet (2,400 IU retinyl palmitate/kg diet) or a vitamin A supplemented diet (200,000 IU retinyl palmitate/kg diet) for 1 mo prior to tumor cell injection to preload the liver with vitamin A. HCT-116, ATRA-resistant, human colon cancer cells were intrasplenically injected. Mice continued to consume their respective diets for 5 wk following surgery. Consumption of supplemental vitamin A decreased hepatic metastatic multiplicity to 17% of control. Hepatic and splenic retinol and retinyl ester concentrations were significantly higher in the mice supplemented with vitamin A when compared to mice consuming the control diet. Supplemental vitamin A did not decrease body weight, feed intake, or cause toxicity. Thus, supplemental dietary vitamin A may decrease the overall number of hepatic metastasis resulting from colon cancer.     

High levels of dietary carnosine are associated with increased concentrations of carnosine and histidine in rat soleus muscle

The aims of this investigation were to: 1) determine the effect of a moderately high dose of carnosine on muscle concentrations of carnosine, histidine and vitamin E at deficient, minimally adequate and sufficient levels of dietary vitamin E and 2) compare the effects of moderately high and pharmacological doses of carnosine on muscle concentrations of carnosine, histidine and vitamin E when dietary vitamin E is minimally adequate. Muscle concentrations of carnosine, histidine and vitamin E were measured in the lateral gastrocnemius and red and white vastus lateralis; carnosine and histidine concentrations were also measured in soleus muscle. Male Sprague-Dawley rats (n = 12/group) were fed a basal vitamin E-deficient diet supplemented with either 0, 0.001 or 0.01% vitamin E and 0, 0.1 or 1.8% carnosine. After 8 wk, 1.8% carnosine resulted in significant fivefold increases in carnosine and twofold increases in histidine in the soleus muscle (P < or = 0.05). Muscle vitamin E concentrations were not significantly affected by dietary carnosine. Thus, very high levels of dietary carnosine are associated with increases in carnosine and histidine concentrations in rat soleus muscle.     

Effects of dietary vitamin E and high level of ascorbic acid on iron distribution in rat tissues

The effects of dietary vitamin E and high-level supplementation of ascorbic acid on iron distribution in rat tissues were studied. Weanling male Sprague-Dawley rats, fed ad libitum a vitamin E and ascorbic acid free basal diet, were divided into four groups. They were supplemented with 0 or 45 IU/kg diet of vitamin E, and O or 0.2% ascorbic acid in a 2 X 2 complete factorial design. After 12 weeks, rats were killed; blood, liver, spleen, heart and skeletal muscle were collected for analysis. Vitamin E deficiency resulted in significantly decreased plasma iron levels and total iron binding capacity. The total iron and nonheme iron contents of the liver and spleen were significantly higher in the vitamin E-deficient groups compared with control groups. Vitamin E or ascorbic acid supplementation had no effect on iron content of the heart. Non-heme iron levels on per gram tissue were highest in the skeletal muscle of the group to which no vitamin E or ascorbic acid were supplemented. It appears that vitamin E and ascorbic acid interactively affect the iron distribution in rat tissues.     

孕期补充维生素D对先天性佝偻病的预防作用

将妊娠28周的受试孕妇随机分为4组,分别1次性口服维生素D(VD)10万IU或肌注VD10万IU或20万IU,对照组口服空白胶囊.结果3个补充组产妇血和脐血25-(OH)D水平以及产妇血钙水平显著高于对照组(P<0.05),而产妇血和脐血25-(OH)D小于27.3nmol/L(11ng/ml)的发生率以及孕后期腿抽筋的发生率显著低于对照组,补充组产妇血25-(OH)D水平高于其妊娠28周时的水平.补充组未发现先天性佝偻病,而对照组先天性佝偻病和可疑先天性佝偻病的发生率显著高于补充组。结果提示孕后期补充VD可明显改善孕妇和胎儿的VD和钙的营养状况.预防先天性佝偻病,品服与肌泣10万IU与20万IU效果相同.     

Hepatic Vitamin A Preloading Reduces Colorectal Cancer Metastatic Multiplicity in a Mouse Xenograft Model

Previous research in our laboratory showed that retinol inhibited all-trans retinoic acid (ATRA)-resistant human colon cancer cell invasion via a retinoic acid receptor-independent mechanism in vitro. The objective of the current study was to determine if dietary vitamin A supplementation inhibited metastasis of ATRA-resistant colon cancer cells in a nude mouse xenograft model. Female nude mice (BALB/cAnNCr-nu/nu, n = 14 per group) consumed a control diet (2,400 IU retinyl palmitate/kg diet) or a vitamin A supplemented diet (200,000 IU retinyl palmitate/kg diet) for 1 mo prior to tumor cell injection to preload the liver with vitamin A. HCT-116, ATRA-resistant, human colon cancer cells were intrasplenically injected. Mice continued to consume their respective diets for 5 wk following surgery. Consumption of supplemental vitamin A decreased hepatic metastatic multiplicity to 17% of control. Hepatic and splenic retinol and retinyl ester concentrations were significantly higher in the mice supplemented with vitamin A when compared to mice consuming the control diet. Supplemental vitamin A did not decrease body weight, feed intake, or cause toxicity. Thus, supplemental dietary vitamin A may decrease the overall number of hepatic metastasis resulting from colon cancer.     

Influence of eicosapentaenoic acid and vitamin E on hepatic hydroxyproline content in rabbits fed cholesterol-rich diet

The effect of eicosapentaenoic acid (EPA) and vitamin E on hepatic hydroxyproline content, as an index of collagen was examined in rabbits receiving cholesterol rich diets for a period of 45 days. Rabbits were divided as control (A) and cholesterol fed groups (B, C, D). Group C received 80 mg. of EPA and group D received 100 IU of vitamin E daily in addition to the cholesterol rich diet (2% w/w) which was solely given to group B. The maintenance of rabbits on high cholesterol diets resulted in significantly increased liver cholesterol concentrations. This effect was most pronounced in rabbits receiving cholesterol alone. Hepatic triglyceride levels remained unchanged in all cholesterol-fed rabbits, but total phospholipid levels in liver significantly decreased in EPA and vitamin E supplemented rabbits. An interesting finding was the increase in hepatic hydroxyproline content in rabbits following the administration of EPA and vitamin E to cholesterol rich diet.     

High dietary iron enhances oxidative stress in liver but does not increase aberrant crypt foci development in rats with low vitamin E status

The purpose of this study was to examine the effects of high-iron and low-vitamin E diets on lipid peroxidation and aberrant crypt foci (ACF) development in rats. In a 2 x 2 x 2 factorial design, male Sprague-Dawley rats were fed 45 or 450 mg Fe/kg diet (adequate and high iron, respectively) and 15 or 100 IU vitamin E/kg diet (low and adequate vitamin E, respectively) for three weeks, when they received saline or azoxymethane (15 mg/kg for 2 wk). Diets were continued for an additional six weeks. Serum alpha-tocopherol concentrations in rats fed low-vitamin E diets were decreased to 30% of concentrations observed in rats fed adequate-vitamin E diets (p < 0.0001). Also, serum alpha-tocopherol concentrations tended to be lower in rats supplemented with iron (p < 0.08). Lipid peroxidation in liver was significantly elevated by high-iron diets after 3 and 10 weeks of treatment, but lipid peroxidation in colonic mucosa was not altered by dietary iron or vitamin E. The total number of ACF and number of large ACF (> or = 4 aberrant crypts/focus) were not significantly altered by iron or vitamin E intakes. However, the size distribution of ACF was slightly altered, such that iron-supplemented rats had 12% more ACF with two crypts per focus (p < 0.02) than rats fed adequate-iron diets. Our data suggest that high-iron diets enhanced oxidative stress in liver, but not colon, of rats fed low-vitamin E diets. Furthermore, a high-iron diet does not increase the total number of ACF, even when vitamin E status is low.     

Maternal vitamin E supplementation affects the antioxidant capability and oxidative status of hatching chicks

The effects of maternal vitamin E supplementation on the antioxidant status of chicks were investigated. Female breeder chicks were fed corn-soybean growing diets without supplemental vitamin E for a 17-wk developmental period. After 17 wk, the birds were randomly assigned to 5 treatments and fed corn-soybean diets supplemented with 0, 40, 80, 120, and 160 mg/kg vitamin E (all-rac-alpha-tocopherol acetate), respectively. Blood samples were collected and pullets were artificially inseminated at 35 wk of age. Eggs laid beginning on d 2 after insemination were placed in an incubator. At the time of hatching, 12 chicks from each treatment were randomly sampled and killed. Livers and brains of chicks were collected for the subsequent evaluation of antioxidant status. Plasma vitamin E concentrations increased linearly (P < 0.001; r = 0.997) with the increase in supplemental vitamin E, but those in egg yolk reached a plateau at 120 mg/kg supplemental vitamin E. The malondialdehyde (MDA) concentration, an indicator of lipid peroxidation, of chick brain decreased linearly (P < 0.01; r = -0.909) with the increase in supplemental vitamin E. Pullets given 160 mg/kg supplemental vitamin E had lower plasma MDA concentrations than those given 0 mg/kg (P < 0.05). Similar results were found for the reactive oxygen species levels, an indicator of oxidative stress, of chick brain and liver. For antioxidant enzymes, chicks of pullets given 120 mg/kg supplemental vitamin E had higher (P < 0.05) activities of liver catalase than those given 0-80 mg/kg. Chicks of pullets given 160 mg/kg supplemental vitamin E had higher (P < 0.05) activities of brain superoxide dismutase than those given 0-40 mg/kg. These results indicated that maternal supplementation with high levels of vitamin E (120-160 mg/kg) enhances antioxidant capability and depresses oxidative stress in chicks.     

三种维生素对仔鸡发育及组织维生素含量的影响

目的：　研究日粮维生素Ａ（ＶＡ）、维生素Ｄ（ＶＤ）、维生素Ｅ（ＶＥ）在营养方面的相互影响。方法：　在基础日粮中添加不同剂量的维生素组成试验日粮进行动物试验,测定肉鸡的增重、饲料转化率和组织维生素含量。　结果：　当饲粮ＶＥ含量为２０ ＩＵ／ｋｇ 时,采食每千克饲粮添加２０ ０００ＩＵ ＶＡ的仔鸡增重显著低于采食每千克饲粮添加１ ５００ＩＵ 的仔鸡（Ｐ＜ ０．０５）;高ＶＡ组鸡的血浆和肝脏ＶＥ含量非常显著低于低ＶＡ组（Ｐ＜ ０．０１）,表明日粮高水平ＶＡ可能抑ＶＥ的吸收;当饲粮ＶＡ含量为３０ ０００ＩＵ／ｋｇ、ＶＥ为２０ＩＵ／ｋｇ 时,随ＶＤ水平极度提高,雏鸡体重呈下降趋势。而饲粮ＶＤ含量为２００ＩＵ和１ ０００ＩＵ／ｋｇ 对鸡生长及血液和肝脏ＶＡ、ＶＥ含量无显著性影响;当ＶＥ水平提高到２００ ＩＵ／ｋｇ,ＶＤ水平提高到８ ０００ ＩＵ／ｋｇ 时,雏鸡体重显著增加（Ｐ＜ ０．０５）;在相同ＶＤ水平下,高水平ＶＥ日粮组试鸡的体重均高于低水平日粮组。结论：日粮ＶＡ、ＶＤ和ＶＥ间存在着显著的相互影响,在配制动物日粮时应注意ＶＡ、Ｄ和Ｅ的适宜比例关系。     

Lung eicosanoid synthesis is affected by age, dietary fat and vitamin E.

The effect of age, dietary fat type and all-rac-alpha-tocopheryl acetate (vitamin E) supplementation on ex vivo synthesis of lung eicosanoids was measured in C57BL/6NIA mice using a 2 (age) x 3 (fat) x 3 (vitamin E) factorial design. Young (3-mo-old) and old (24-mo-old) mice were fed a semipurified diet containing 5% (by wt) corn oil, coconut oil or fish oil supplemented with 30, 100 or 500 mg vitamin E/kg for 4 wk. Ex vivo synthesis of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (PGI2) were measured by RIA in lung homogenates. Old mice had significantly higher concentrations of TXB2 and PGI2 than did young mice, resulting in a significant increase in the TXB2:PGI2 ratio with aging. Young and old mice fed fish oil had significantly lower concentrations of PGI2 and TXB2 than those fed corn oil or coconut oil. The degree of reduction varied according to age and vitamin E status. Old mice fed fish oil and 30 mg vitamin E/kg diet had the lowest plasma vitamin E concentration and the highest TXB2:PGI2 ratio. The TXB2:PGI2 ratio was significantly reduced in old mice fed coconut oil or fish oil by vitamin E supplementation. Vitamin E supplementation (100 mg/kg) significantly increased PGI2 concentration in young mice fed coconut oil. Thus, significant changes in the capacity of lung to synthesize eicosanoids occur with age and are influenced by dietary fat type and vitamin E. J. Nutr.     

Oral tocotrienols are transported to human tissues and delay the progression of the model for end-stage liver disease score in patients

The natural vitamin E family is composed of 8 members equally divided into 2 classes: tocopherols (TCP) and tocotrienols (TE). A growing body of evidence suggests TE possess potent biological activity not shared by TCP. The primary objective of this work was to determine the concentrations of TE (200 mg mixed TE, b.i.d.) and TCP [200 mg α-TCP, b.i.d.)] in vital tissues and organs of adults receiving oral supplementation. Eighty participants were studied. Skin and blood vitamin E concentrations were determined from healthy participants following 12 wk of oral supplementation of TE or TCP. Vital organ vitamin E levels were determined by HPLC in adipose, brain, cardiac muscle, and liver of surgical patients following oral TE or TCP supplementation (mean duration, 20 wk; range, 1-96 wk). Oral supplementation of TE significantly increased the TE tissue concentrations in blood, skin, adipose, brain, cardiac muscle, and liver over time. α-TE was delivered to human brain at a concentration reported to be neuroprotective in experimental models of stroke. In prospective liver transplantation patients, oral TE lowered the model for end-stage liver disease (MELD) score in 50% of patients supplemented, whereas only 20% of TCP-supplemented patients demonstrated a reduction in MELD score. This work provides, to our knowledge, the first evidence demonstrating that orally supplemented TE are transported to vital organs of adult humans. The findings of this study, in the context of the current literature, lay the foundation for Phase II clinical trials testing the efficacy of TE against stroke and end-stage liver disease in humans.     

Effects of ergocalciferol supplementation on the concentration of vitamin D and its metabolites in human milk

The effect of maternal ergocalciferol (vitamin D2) supplementation on the concentrations of vitamin D, 25-hydroxyvitamin D (25-OH-D), 24R,25-dihydroxyvitamin D [24,25-(OH)2D], and 1 alpha,25-dihydroxyvitamin D [1,25-(OH)2D] in their milk was studied. Vitamin D2, D3, 25-OH-D2 and 25-OH-D3 were simultaneously determined by high performance liquid chromatography, and the determination of 24,25-(OH)2D and 1,25-(OH)2D was performed by competitive protein binding assay and radioreceptor assay, respectively, after separation of the D2 and D3 compounds. After healthy lactating mothers had received a daily oral dose of vitamin D2 (1,200 IU/d) for 4 wk, the concentrations of vitamin D2, D3 and the metabolites were determined in their plasma and milk. Although the plasma levels of 25-OH-D2 were significantly increased, the increase in milk was relatively small. On the other hand, the increase of vitamin D2 levels in milk was greater than that of 25-OH-D2 in milk after supplementation. The levels of 1,25-(OH)2D in milk was lower after 5 wk of lactation than after 1 wk of lactation, regardless of maternal vitamin D2 supplementation. When total antirachitic activities in milk were calculated, only a very slight increase was observed as a result of supplementation.     

Effect of dietary polyunsaturated/saturated fatty acid ratio and dietary vitamin E on lipid peroxidation in the rat

The effects of the dietary ratio of polyunsaturated/saturated fatty acids (P/S) and dietary vitamin E on lipid peroxidation (LP) were examined to determine whether the vitamin E requirement is elevated by increased P/S in ratios comparable to those found in human diets. Twelve groups of male weanling rats (six/group) were fed purified diets containing 20% fat with P/S ratios of 0.38, 0.82 or 2.30. At each P/S level, groups of rats received either 0, 10, 40 or 100 IU vitamin E/kg diet supplied as all-rac-alpha-tocopherol. After the diets were fed for 16 wk, in vivo LP was assessed by measuring pentane in expired breath. Pentane levels were significantly elevated in rats fed 0 IU vitamin E at all P/S levels. Both 40 and 100 IU vitamin E decreased pentane production to minimal levels for all P/S groups. Liver malondialdehyde levels and in vitro spontaneous red blood cell hemolysis results also indicated a significant effect of vitamin E in reducing in vitro LP, but no overall effect of P/S. Testicular and epididymal histology showed no effect of dietary P/S on the vitamin E requirement. These data demonstrated 40 IU vitamin E to be adequate for maximal inhibition of LP at the P/S levels tested and indicated that these levels of dietary P/S had no significant impact on the vitamin E requirement for the growing rat.     

补充维生素A与铁对改善学龄前儿童贫血和免疫功能的影响

目的为观察学龄前儿童亚临床维生素A(VA)缺乏状态缺铁时,机体免疫功能的变化以及VA与铁同时补充对改善儿童铁营养状况和免疫功能的影响.方法检测北京农村270名3～7岁儿童血清VA含量和血红蛋白(Hb)、血清铁(SI)、运铁蛋白饱和度(TS)及血清铁蛋白(SF)后,将其分为正常、低 VA、低铁和低VA低铁4组,每组选40人,检测血清免疫球蛋白IgA、IgG、IgM 与白细胞介素-2(IL-2).然后将低VA低铁组儿童随机分为补铁组 (每日口服相当于30 mg元素铁的硫酸亚铁,连续8周)和补VA+铁组(口服VA胶丸12 500 IU /次,2次/周,连续8周;口服铁量同补铁组,连续8周),分别进行干预.干预后重复检测血清VA、血液铁生化指标和以上免疫指标,进行两组间比较,并与干预前比较. 结果低VA低铁组儿童血清IgM为(1 260±310) mg/L显著高于正常组的(1 0 7 0±170) mg/L.对其实施VA+铁联合干预后,血清TS为(26.5±8.6)%,明显高于补铁前的(16.2±1.6)%和单纯补铁组的(22.3±3.8)%;IL-2在VA与铁同时补充后为(2 78.9±117.7) ng/L,显著高于补充前的(161.6±90.3) ng/L和单纯补铁组的(189 .5 ±89.3)ng/L的水平;其他铁生化指标和免疫指标无明显变化.结论对存在亚临床VA缺乏状态的缺铁儿童实施一定剂量的VA+铁联合干预,对改善机体铁营养状况和免疫功能有明显作用.