Serum Tocopherol Levels Research Articles

Association between serum vitamin A and E levels and HIV-1 disease progression.

To examine the associations between serum vitamin A and E levels and risk of progression to three key outcomes in HIV-1 infection: first AIDS diagnosis, CD4+ cell decline to < 200 cells x 10(6)/l, and mortality. Non-concurrent prospective study. Serum levels of vitamins A and E were measured at the enrollment visit of 311 HIV-seroprevalent homo-/bisexual men participating in the Baltimore/ Washington DC site of the Multicenter AIDS Cohort Study. Cox proportional hazards models were used to estimate the relative hazard of progression to each outcome over the subsequent 9 years, adjusting for several independent covariates. Men in the highest quartile of serum vitamin E levels (> or = 23.5 mumol/l) showed a 34% decrease in risk of progression to AIDS compared with those in the lowest quartile [relative hazard (RH), 0.66; 95% confidence interval (CI), 0.41-1.06)]. This effect was statistically significant when comparing the highest quartile of serum vitamin E to the remainder of the cohort (RH, 0.67; 95% CI, 0.45-0.98). Associations between serum vitamin A levels and risk of progression to AIDS were less clear, but vitamin A levels were uniformly in the normal to high range (median = 2.44 mumol/l). Similar trends were observed for each vitamin with mortality as the outcome, but neither vitamin was associated with CD4+ cell decline to < 200 cells x 10(6)/l. Men who reported current use of multivitamin or single vitamin E supplements had significantly higher serum tocopherol levels than those who were not taking supplements (P = 0.0001). Serum retinol levels were unrelated to intake of multivitamin or single vitamin A supplements. These data suggest that high serum levels of vitamin E may be associated with slower HIV-1 disease progression, but no relationship was observed between retinol levels and disease progression in this vitamin A-replete population.

馬の胎盤排泄時間に及ぼすビタミンEの投与効果

The effect of vitamin E (1, 000 mg) injected intramuscularly once, twice or three times at 5-day intervals several days before parturition on excretion hours of fetal membrane in mares was examined. In the group with no treatment of vitamin E, the rates of mares with fetal membrane excretion over 60 minutes were 11.1% of the group above 300μg/100 ml of serum tocopherol levels, but 33.3% in the mares below 300μg/100 ml. In the group with vitamin E injection, all mares showing low levels of serum tocopherol below 300μg/100 ml excreted the fetal membrane within 60 minutes, and the hours were significantly (p<0.05) less than the non-treated group. The serum selenium and blood glutathione peroxidase activities of the mares examined were at normal levels, and were not related to the times of fetal membrane excretion.

乳用雄子牛と雌子牛の発育段階における血清のビタミンA, ビタミンE, セレニウム, 脂質分画および血液グルタチオンペルオキシダーゼ活性の変化

Ninety bull calves for fattening and thirty heifer calves of the Holstein breed were classified into five growth stages (stage I: 7 days old; stage II: 1 month old; stage III: 3 months old; stage IV: 6 months old; stage V: 12 months old; stage VI: 17 to 18 months old) and blood chemical components including serum lipid fractions, vitamin A, vitamin E (tocopherol), selenium and blood glutathioneperoxidase activity were examined during each of these growth stages.During the fattening stage (stage V to VI) of bull calves, serum lipid fractions including total lipid, phospholipid, total cholesterol, ester cholesterol and lipid peroxide, and serum tocopherol levels increased significantly compared with the levels of heifer calves in the same growth stages, but the levels of serum retinol and erythrocyte tocopherol decreased to the contrary. There were many correlations between the level of serum tocopherol and the serum lipid compositions including phospholipid, total cholesterol and total lipid. The increase in the serum lipid levels during the fattening stage of bull calves seemed to reflect the development of the fatty tissue. Also, the decrease in erythrocyte tocopherol which is an indication of bioavailable tocopherol might be caused by the increase in the shift to fatty tissue of tocopherol.The serum selenium level and blood glutathioneperoxidase activity decreased markedly from stage V to VI for the heifer calves, and it was suggested that the decrease in both blood components was due to the low selenium diet.

Effect of dietary canola and reference oils upon serum lipids and platelet aggregation

To compare Canola a terrestrial (n-3) oil with fish oil (n-3) and common vegetable oil (n-6) in decreasing serum lipids and platelet aggregation, various oils were included in Chow ®-based diets and fed to rats in an eight-weeks feeding trial. The Chow ® diet contained 2% cholesterol along with either Canola, menhaden, safflower, or partially hydrogenated soy oil, or no oil addendum. The menhaden oil group was the only one to show a significant reduction in serum cholesterol and triglycerides and at the same time yielded the most uniform decrease in platelet aggregability. However, this same group was also the only one to show a decrease in serum tocopherol levels, suggesting that improving an atherogenic risk profile may require antioxidant supplementation. In these rat trials, Canola oil supplementation did not yield the same results measured during menhaden supplementation.

Effect of excess dietary copper, iron or zinc on the tocopherol and selenium status of growing pigs.

Two experiments were conducted to evaluate the effect of the addition of high levels of Cu (as CuSO4), Fe (as FeSO4) or Zn (as ZnO) to swine starter and grower diets on performance and vitamin E and Se status. The stability of natural tocopherols in mixed feeds was evaluated during storage. Addition of 1,000 ppm Fe or 1,000 ppm Zn had no effect on rate or efficiency of weight gain in either experiment. In Exp. 1, the addition of 250 ppm Cu improved daily gain and efficiency of feed utilization (P less than .05) during the first 3 wk of the experiment. Copper had no effect on pig performance during the rest of Exp. 1 or in Exp. 2. Serum lactate dehydrogenase or glutathione peroxidase activity was not affected (P greater than .1) by any of the mineral additions. Serum tocopherols were not affected by the mineral treatments in Exp. 1. In Exp. 2, addition of 250 ppm Cu decreased (P less than .01) serum tocopherol levels throughout the 8-wk experiment. The alpha-tocopherol levels of the starter diet decreased (P less than .05) during storage. Addition of 250 ppm Cu (P less than .01) or 1,000 ppm Fe (P less than .05) or 1,000 ppm Zn (P less than .05) increased the destruction of alpha-tocopherol in the starter diet. Alpha- and gamma-tocopherol levels of the starter diet decreased to near zero in 22 d in the presence of 250 ppm Cu. In the grower diet, the addition of 250 ppm Cu (P less than .01) or 1,000 ppm Fe (P less than .05) increased the destruction of tocopherols.(ABSTRACT TRUNCATED AT 250 WORDS)

Studies on serum tocopherol and selenium levels and blood glutathione peroxidase activities in lambs with white muscle disease.

For the investigation of the cause of white muscle disease (WMD), tocopherol (Toc) and selenium (Se) levels and blood glutathione peroxidase (GSH-Px) activities were examined using lambs with WMD and their ewes. Serum Se levels of 4 lambs with WMD were low under 30 ppb, lambs showing very low levels below 15 ppb. The serum Se level was correlated with blood GSH-Px activity showing remarkably low activities in the lambs with WMD. Se contents in the organs of lambs with WMD were lower than those of control lambs, and particularly liver Se contents were deficient levels below 50 ppb. Serum Toc levels were normal, but alpha-Toc contents in organs showed very low levels, especially in the liver. The serum Toc and Se levels and blood GSH-Px activities of their ewes and other sheep kept in the same farm revealed similar results to those of lambs with WMD. Feedstuffs supplied on the farm showed the deficient level of the Se content below 50 ppb and a very low level of alpha-Toc. It was concluded that WMD of lambs in Hokkaido was nutritional muscular dystrophy resulted from deficiencies of Toc and Se to their ewes.

子牛へのビタミンAD&lt;SUB&gt;3&lt;/SUB&gt;Eプレミックス投与に対する胆汁分泌促進処置の効果

In order to recognize the relationship of bile secretion and related blood levels after oral administration of fat soluble vitamins in calves, changes in serum tocopherol and vitamin A levels were examined in two groups, one administered only vitamin AD3E (AD3E group) and another receiving both vitamin AD3E and cholagogue (cohlagogue group).In the calves who were administered 1, 000 IU of vitamin E orally, increased serum tocopherol levels after the administration continued for 8 to 24 hours in the AD3E group and for 8 to 48 hours in the cholagogue group. In the calves orally administered 2, 000 IU of vitamin E an increase of serum tocopherol levels continued for 8 to 24 hours in the AD3E group and for 8 to 72 hours in the cholagogue group. In addition, the increased rate of serum tocopherol level was higher in the cholagogue group than in the AD3E group. In the calves orally administered 2, 500, 000 IU of vitamin A the rate increase of serum retinyl palmitate level was higher in the cholagogue group than in the AD3E group.From the findings described above, it was considered that cholagogue is effective for promotion of intestinal absorption of vitamin E and A administered orally in calves.

Studies on serum tocopherol, selenium levels and blood glutathione peroxidase activities in calves with white muscle disease.

For the purpose of clarifying the cause of white muscle disease (WMD) in calves, tocopherol and selenium levels and blood glutathione peroxidase (GSH-Px) activity were measured on 10 calves with WMD and nine of their dams. The main clinical symptoms of the 10 calves with WMD were motor disturbances including recumbency and stiffness. Serum enzyme activities (GOT, GPT, CPK, LDH) in calves with WMD increased markedly, and this increase was also observed in some of their dams. Serum tocopherol levels of calves with WMD were low, 70% of which showing deficient levels of less than 70 micrograms/100 ml. Serum selenium levels of all the calves were lower than 35 ppb, indicating a deficiency, and were accompanied by low blood GSH-Px activity. alpha-Tocopherol and selenium concentrations in organs were very low. Dams of calves with WMD showed low serum tocopherol levels, 22% of which indicating deficient levels below 150 micrograms/100 ml. Serum selenium levels in dams showed a marked decrease to under 20 ppb, and also low blood GSH-Px activity. Feedstuffs supplied in the farms to affected calves indicated very low alpha-tocopherol contents (below 3 mg/100g DM) and low selenium concentrations below 50 ppb in DM. It was concluded that WMD in calves was attributable to nutritional muscular dystrophy caused by deficiencies in tocopherol and selenium in feedstuffs supplied to their dams.

Studies on serum selenium and tocopherol in white muscle disease of foal.

In order to clarify the cause of white muscle disease (W.M.D.) in foals, tocopherol and selenium concentrations in serum and glutathione peroxidase activities in blood were measured. Examination was made on the samples from horses affected with W.M.D., the foal kept with them in the same stable, the foals kept in the stables without affected foals, and respective mares. The heavy-breed horses in Fukuoka prefecture and Tokachi district were also examined for comparison. Serum tocopherol levels of these foals were normal because after intake of colostrum. Mares of affected foals showed lower tocopherol levels than other examined mares (p less than 0.01). Serum selenium levels of all foals were below 65 ppb, showing deficient levels. The mares of affected foals had lower selenium levels than other mares (p less than 0.01). There was a good correlation between serum selenium concentration and blood glutathione peroxidase activity (r = 0.81). Selenium levels in the liver of affected foals were lower than the foals which succumbed with other diseases. Diet supplied in the stables with affected foals showed low alpha-tocopherol and selenium contents. These findings suggest that W.M.D. in foals is attributed to nutritional muscular dystrophy caused by tocopherol and selenium deficiency of their mares in late gestation period.

Effect of Vitamin E Usage on Serum Tocopherol, Total Serum Lipids, Retinol and Carotene in Retired Citizens

A study was conducted to compare selected biochemical variables in 80 non-institutionalized retired citizens relative to supplemental vitamin E intake, sex and age. No low levels of either serum tocopherol or serum retinol existed in any of the subjects, whereas high levels were present in both the supplemental and non-supplemental vitamin E population. The supplemental vitamin E group had a significantly higher mean serum tocopherol level than the non-supplemental E group. In the subjects who took vitamin E supplements, positive correlations were observed between serum tocopherol and the parameters of total serum lipids, serum carotene and serum retinol and between serum retinol and total serum lipids. In the non-supplemental vitamin E subjects, serum tocopherol was related to total serum lipids. In both groups, mean levels of total serum lipids were higher in men than women, with a significant difference in the non-supplemental group. The younger age (58 to 70 years) group taking vitamin E supplements t...

Serum Vitamin E Levels in the Very Low Birth Weight Infant During Oral Supplementation

A prospective study was initiated to monitor serum tocopherol levels in all infants admitted to Indiana University Medical Center with birth weights less than 1,500 g. These infants routinely receive 100 mg/kg/d of oral vitamin E (Aquasol E tocopherol acetate) every six hours. Levels are determined weekly or semiweekly using a modification of the fluorometric method of Hanson and Warwick. Vitamin E dosage is adjusted regularly to achieve levels greater than or equal to 3.5 mg/dL. During the 6 months of this study, a total of 76 patients had 567 serum measurements. Of these, 220 levels (38%) were greater than or equal to 3.5 mg/dL, 71 (13%) were greater than or equal to 5.5 mg/dL, and 15 (2.7%) were greater than 8 mg/dL. Serum tocopherol levels often (1) remained greater than or equal to 3.5 mg/dL for several days after oral supplementation was discontinued or (2) again became greater than or equal to 3.5 mg/dL on a reduced dosage of 25 to 50 mg/kg/d. These data indicate that infants weighing less than 1,500 g at birth who are receiving oral vitamin E supplementation at 100 mg/kg/d will have varied serum levels with a significant percentage exceeding 3.5 mg/dL.

1466 SERUM VITAMIN E LEVELS IN THE VERY LOW BIRTH WEIGHT INFANT DURING ROUTINE ORAL SUPPLEMENTATION

A prospective study was initiated to monitor serum tocopherol levels in all infants admitted to Indiana University Medical Center with birth weights 3.5 mg/dL. During the first 10 weeks of study, a total of 52 patients had 320 serum measurements. Of these, 132 levels (41%) were >3.5 mg/dL, and 42 (13%) were >5.5 mg/dL. Among 27 patients weighing 500-1000 grams, 87 of 197 levels (44%) were >3.5 mg/dL. Among 25 patients weighing 1001-1500 grams, 45 of 123 levels (37%) were 3.5 mg/dL. Serum tocopherol levels often: a) remained >3.5 mg/dL for several days after oral supplementation was discontinued, or b) again became >3.5 mg/dL on a reduced dosage of 25-50 mg/kg/day. These data indicate that infants weighing <1500 grams at birth who are receiving oral vitamin E supplementation at 100 mg/kg/day will have varied serum levels with a significant percentage exceeding 3.5 mg/dL.

正常馬における血清トコフェロールの変動

正常馬における血清トコフェロールの変動

Dietary Supplementation with Vitamin E in Hyperlipoproteinemias: Effects on Plasma Lipid Peroxides, Antioxidant Activity, Prostacyclin Generation and Platelet Aggregability

In a placebo-controlled trial healthy volunteers and patients with hyperlipoproteinemias types II and IV received orally vitamin E at doses of 300 mg and 600 mg daily for 2 weeks. Serum tocopherol levels increased two-fold, but serum concentrations of total lipids, cholesterol, triglycerides, ceruloplasmin and transferrin remained unchanged. Dietary supplementation with vitamin E suppressed elevated concentrations of plasma lipid peroxides and this effect was correlated with an increase in serum antioxidant activity. In patients a mild platelet suppressant effect of vitamin E (600 mg daily) was observed. Feeding an atherogenic diet to rabbits for a week resulted in elevation of plasma lipid peroxides and a 90% decrease in arterial generation of prostacyclin. Enrichment of the atherogenic diet with 100 mg vitamin E daily prevented the increase in plasma lipid peroxides and protected the prostacyclin generating system in arteries. Thus, in hyperlipoproteinemias vitamin E corrects certain abnormalities of lipid metabolism which might predispose to atherosclerosis.

Vitamin E and Necrotizing Enterocolitis

Although vitamin E has been shown to reduce the incidence of severe sequelae from retrolental fibroplasia, there have been recent suggestions that its use may be associated with an increased incidence of necrotizing enterocolitis (NEC). A review was made of experience with vitamin E, both intramuscular and oral, and NEC over a 4 1/2-year period. Of 418 infants of birth weight less than 1,500 g admitted during this period, 28/209 infants who had received vitamin E had definite NEC (13.4%) compared with 12/209 who had not received vitamin E (5.74%, chi 2 = 7.07, P = .008). For infants of birth weight less than 1,250 g, 16/103 infants who received vitamin E developed NEC v 1/159 who had not (chi 2 = 21.1, P less than .001); the incidence of NEC was not significantly different between the two groups for infants with birth weight between 1,250 to 1,500 g. The early mortality (less than seven days) for infants with birth weight of 1,500 g or less was significantly greater for those who had not received vitamin E (43.5% v 13.8%, chi 2 = 44.9, P less than .001), most probably a reflection of the omission of this drug for the most critically ill infants in this retrospective review. The incidence of NEC was not different for infants with birth weight of 1,500 g or less who received intramuscular vitamin E compared with control infants from the same period. For those infants for whom serum tocopherol levels were available, no infant who developed NEC and who had received only oral vitamin E had a serum tocopherol levels of greater than 3.5 mg/100 mL.(ABSTRACT TRUNCATED AT 250 WORDS)

Study on Cystic Fibrosis Criticized

To the Editor.— The study design and data of Ater et al1 do not justify the authors' conclusion that iron deficiency contributes to relative anemia in patients wih cystic fibrosis. The statistically significant (but meager) increase in hemoglobin concentration in their study came only after vitamin E was added to the regimen of oral iron. They apparently assume that since an increase in hemoglobin could not be correlated with an initially low serum tocopherol level, the vitamin E supplementation had no effect.

Effect of Vitamin E as an Immunopotentiation Agent for Mice at Optimal Dosage and Its Toxicity at High Dosage

Studies have been done to determine the optimal dosage of vitamin E. Vitamin E is generally considered to be relatively nontoxic at high dosage in spite of the fact that it is a fat-soluble vitamin. From our experiments using mice, when various dosages of all-rac-α-tocopherol were injected into the intraperitoneal cavity every day, 1) the body weight decreased when the dose was more than 100 iu/kg per day, and all the mice died within 3 days at 400 iu/kg per day; 2) immune responses investigated by lymphoproliferative assays with phytohemagglutinin, concanavalin A and lipopolysaccharide were enhanced significantly between 5 and 20 iu/kg per day, but were inhibited by 80 iu/kg per day. when the immunopotentiation effect of vitamin E was discernible, serum tocopherol levels were about twice the control values. From our results, the optimal dosage of vitamin E was between 5 and 20 iu/kg per day, and dosages over 80 iu/kg per day were toxic to mice. We then experimented similarly with vitamin K, which is fat soluble and possesses a quinone structure resembling vitamin E. When doses between 12.5 and 150 mg/kg per day of vitamin K were injected into the intraperitoneal cavity daily for 14 days, increase of body weight was generally inhibited. This did not depend on the dose, and there was no definite relationship between mitogen responses and vitamin K.vitamin E vitamin K mitogen response immunopotentiator toxicity

Effects of the Source of Dietary Protein on Serum Lower Density Lipoprotein (VLDL + LDL) and Tocopherol Levels in Female Rats

The effect of dietary protein on lipid levels of serum and liver and mineral contents of bone tissue was studied in female rats by using 13 semi-purified diets differing with respect to protein source. The diets were characterized with regard to contents of protein, amino acids, fat, crude fiber, phytate, zinc, copper, iron, magnesium, calcium, sodium, potassium, tocopherol and metabolizable energy. Six of the proteins tested were of animal origin and six proteins used were plant proteins. Each diet was fed at a 20% protein, 10% fat level. There was a large variation between groups in the serum content of lower density lipoproteins (VLDL + LDL). Rats fed plant protein diets showed values in a lower range than rats consuming animal protein diets. Triglyceride values showed a similar tendency. A comparison of dietary amino acid composition and blood lipid parameters revealed a significant negative correlation between dietary arginine content and serum VLDL + LDL levels (r = 0.863; P < 0.01). Group differences in total serum cholesterol were also observed. However, this variation was within the same range in animal as well as plant protein diets. Serum tocopherol levels were correlated to the total dietary intakes of tocopherol. No significant trend was observed for the mineral content of bone tissue or for the total lipid content of liver with regard to class of dietary protein. However, all rats fed a blood protein diet developed fatty livers.

Consequences of Vitamin-E Deficiency on the Phagocytic and Oxidative Functions of the Rat Polymorphonuclear Leukocyte

Vitamin E serves an important role in protecting the cellular membrane constituents from peroxidative damage. Biochemical and functional studies were performed on polymorphonuclear leukocytes (PMN) from vitamin-E deficient and control rats to investigate the consequences of uncontrolled peroxidation of the rat PMN membrane. Rats fed a vitamin-E-doficient diet for 2 mo had serum tocopherol levels of only 5.1% of control and exhibited a twofold increase in membrane polyunsaturated fatty acid (PUFA) peroxidation as measured by malonaldehyde production. As a consequence of vitamin-E deficiency, chemotaxis in response to bacterial culture filtrate was deficient. Ingestion was also impaired when saturating concentrations of IgG- and C3b-coated and unopsonized albumin-coated paraffin oil droplets were employed, and ingestion remained deficient when performed in an anaerobic environment. The altered chemotaxis and ingestion in the deficient PMN were restored to normal by 18 hr following the parenteral administration of vitamin E. The deficient PMN ingested and killed C3b-coated Staphylococcus aureus 502-A normally when the bacteria-to-cell ratio was no more than 10:1. Oxygen consumption and hydrogen peroxide release were enhanced in the phagocytosing vitamin-E-deficient PMN. Depletion of vitamin E did not lead to impairment of adherence, surface polarization of concanavalin A into caps, or lysosomal enzyme release. These latter functions are subserved by glutathione-responsive microtubules as well as by actomyosin-containing microfilaments. Thus, the consequences of vitamin-E deficiency in PMN were selective to those areas of the membrane involved in triggering chemotactic, ingestive, and oxidative responses.

Ethane production and liver necrosis in rats after administration of drugs and other chemicals

Lipid peroxidation and liver necrosis due to a number of drugs and chemicals were studied. The agents were administered to control, vitamin E-deficient, and selenium-deficient rats. Vitamin E deficiency was documented by a low serum tocopherol level (0.34 mg/100 ml) and selenium deficiency by a specific activity of the selenoenzyme glutathione peroxidase in 105,000 g liver supernatant which was approximately 1% of the control value. Glutathione S-transferase specific activity, measured with 1-chloro-2,4-dinitrobenzene as substrate, was doubled by selenium deficiency. Ethane production was measured as the index of in vivo lipid peroxidation. Hepatic necrosis was assessed histologically and by measuring serum glutamic-pyruvic transaminase. When no agents were administered, vitamin E-deficient rats produced more ethane than did control or selenium-deficient rats. Phenobarbital did not cause an increase in ethane production. CCl 4 (60 μl/100 g) and BrCCl 3 (5 μl/100 g) caused large ethane production and moderately severe liver necrosis. The vitamin E-deficient and selenium-deficient groups given BrCCl 3 produced more ethane than the controls but had no more severe hepatic necrosis than the controls. Thioacetamide (5 mmol/kg) and acetaminophen (3 g/kg) caused moderate to severe liver necrosis but only small ethane production. Vitamin E deficiency potentiated acetaminophen hepatotoxicity and selenium deficiency inhibited it. Iodipamide (1.5 mmol/kg) caused very large ethane production and death within hours in vitamin E-deficient rats. At a dose of 2 mmol/kg it caused severe liver necrosis in control rats but only small ethane production. This dose caused no liver necrosis in selenium-deficient rats. Acetylhydrazine (30 mg/kg) caused moderate ethane production in all groups but no liver necrosis. A single dose of ethanol (0.68 ml/100 g) led to small production of ethane in all groups. This study shows that many agents are capable of causing in vivo lipid peroxidation, but that lipid peroxidation does not always correlate with liver necrosis. Selenium deficiency is not a simple glutathione peroxidase deficiency state, as hepatic glutathione S-transferase is increased by it and it protects against acetaminophen and iodipamide hepatotoxicity.