Lipoperoxides in organs of vitamin E deficient rats fed large amounts of highly unsaturated fats.

Rats were fed diets containing 10% cod liver oil with and without a supplement of tocopherol acetate for 32 weeks. The determination of peroxides in lipid extracts of adipose tissue, liver, heart and skeletal muscle by different methods was attempted. High amounts of peroxides were found only in adipose tissue of vitamin E deficient animals. Small values were found in other tissues of both groups. The problem whether the organs contain true lipoperoxides, or some other substances are responsible for the peroxide estimates, is discussed.     

Influence of excess vitamin E on vitamin A toxicity in rats.

Male Holtzman rats (78 g) were fed semipurified 16% protein diets for 8 weeks using a food grade soy protein concentrate as the protein source. The basal diet (A) contained added DL-methionine (0.26%) and adequate amounts of vitamins A (14,535 IU/kg as retinyl acetate) and E (60 IU/kg as DL-alpha-tocopheryl acetate) and all other required nutrients. Experimental diets included: (B) basal plus 600 IU of vitamin E/kg; (C) basal plus 6,000 IU of vitamin E/kg; (D) basal plus 2.9 X 10(6) IU of vitamin A/kg; (E) basal plus 2.9 X 10(6) IU of vitamin A plus 600 IU of vitamin E/kg; and (F) basal plus 2.9 X 10(6) IU of vitamin A plus 6,000 IU of vitamin E/kg. Both vitamin A and vitamin E had a significant (P less than 0.05) effect on growth. There was an increase in growth with vitamin E intake and a decrease in growth with vitamin A intake. The net result of these two effects was that the groups fed both vitamins tended to be quite close in mean values to the group fed only the basal diet. Vitamin A significantly (P less than 0.05) increased relative weights of spleen and testes; vitamin E reduced that effect. Vitamin E also significantly (P less than 0.05) reduced relative adrenal weight whereas vitamin A significantly increased it. The two effects tend to cancel each other in the sense that the group fed both vitamins had an average relative adrenal weight quite close to that of the group fed only the basal diet. However, vitamin A still had an effect even when 6,000 IU of vitamin E was fed. The interaction effect of the two vitamins was significant (P less than 0.05) for plasma total protein and liver vitamin A. There was an increase in liver vitamin A with increasing levels of vitamin E in the diet. Blood urea nitrogen and plasma cholesterol were unchanged. A significant interaction of vitamins A and E was found to effect plasma total protein, liver vitamin A, and relative weight of spleen and testes.     

Bioavailability of vitamin E in rats fed graded levels of pectin

Dietary pectin at levels of 0, 3, 6 and 8% was fed ad libitum to rats for 8 wk to evaluate whether the bioavailability of vitamin E fed at 0.001% of the diet was affected by pectin. Rats fed 3% pectin were not different in any vitamin E parameters from those fed 0% pectin. By the end of the study body weights were significantly lower in the 6 and 8% pectin groups after adjusting for their nonsignificant trend of lower food intake. At wk 8, liver vitamin E levels were reduced in the 6 and 8% pectin group compared to values at the start of the study. Both groups had significantly higher red blood cell hemolysis compared to 0% pectin at 8 wk. Fecal fat excretion was not different among the diet groups, but weights of the small and large intestines were significantly increased in rats fed 6 or 8% pectin compared to those fed 0 or 3%. Our results show that 6 and 8 but not 3% dietary pectin decreased vitamin E availability in rats.     

Dietary vitamin E and beta-carotene sources influence vitamin A and E storage in young rats fed marginal and adequate vitamin E

The effects of two vitamin E levels (30 and 75 IU/kg diet) and the interrelation of two vitamin E sources [dl-alpha-tocopheryl acetate (dl-alpha-TA) and d-alpha-tocopheryl acid succinate (d-alpha-TAS)] and three vitamin A sources [retinyl palmitate (RP), all-trans synthetic beta-carotene (SBC), and natural beta-carotene (NBC)] were studied. Dietary vitamin A sources provided 4,000 IU/kg. Twelve groups of Fischer 344 rats (10/group) were fed designated diets for eight weeks. For RP, SBC, and NBC, the increase in each vitamin E source from a marginal to an adequate dietary level caused a significant increase in liver and heart alpha-tocopherol. Among rats fed diets with an adequate level of vitamin E, d-alpha-TAS was not as effective as dl-alpha-TA in increasing liver alpha-tocopherol levels. Plasma retinol was lower in rats fed d-alpha-TAS than in those fed dl-alpha-TA. Among rats fed diets with an adequate level of dl-alpha-TA, those fed SBC had significantly higher liver and heart alpha-tocopherol concentrations than did all other groups (p < 0.05). Liver retinol equivalents for rats fed NBC were approximately 66% lower than those in rats fed SBC or RP (p < 0.05). The roles of the two vitamin E sources in alpha-tocopherol metabolism are not equivalent. These data indicate that vitamin A source influences the magnitude of the tissue vitamin A and E changes in response to the two vitamin E sources.     

RNA synthesis in liver nuclei of young rats fed varying amounts of vitamin A.

Twenty five days old male rats were feed 5000, 20000 and 40000 I.U. of vitamin A for two days and its effects studied on RNA contents and its synthesis from orotic acid-6(-14)C in liver and its nuclear and mitochondrial fractions. RNA contents and its synthesis from orotic acid-6(-14)C in liver, its nuclear and mitochondrial fractions was not affected in rats 5000 I.U. of vitamin A, but these were reduced in rats fed 20000 and 40000 I.U. of vitamin A. The turnover rate of nuclear RNA was significantly greater in rats fed 5000 I.U. of vitamin A as compared to the controls.     

Effects of megadoses of dietary vitamin E on the antioxidant status of rats fed lard or salmon oil

This study was undertaken to investigate whether megadoses of vitamin E in the diet of rats can have pro-oxidative activity. Two experiments with rats were conducted in which both the dietary vitamin E concentration (Experiment 1: 100; 500; 3000; 10,000 mg all-rac-alpha-tocopheryl acetate/kg, and Experiment 2: 100; 1000; 10,000 mg all-rac-alpha-tocopheryl acetate/kg) and the type of dietary fat (lard vs. salmon oil) were varied. Experimental parameters were the concentrations of thiobarbituric acid-reactive substances, 7 beta-hydroxycholesterol, the activities of several antioxidative enzymes, the concentration of glutathione in the liver, and the lag time during copper-induced low-density lipoprotein (LDL) oxidation. Increasing the dietary vitamin E concentration to 10,000 mg all-rac-alpha-tocopheryl acetate/kg led to a significant reduction of thiobarbituric acid-reactive substances in the liver after feeding salmon oil, and also to a significant reduction in 7 beta-hydroxycholesterol after feeding both dietary fats. Megadoses of vitamin E (3000 and 10,000 mg all-rac-alpha-tocopheryl acetate/kg) also led to a reduction in the activity of superoxide dismutase and the concentration of glutathione in the liver of rats fed salmon oil. The lag time during LDL oxidation was independent of the dietary vitamin E concentration. The study shows that megadoses of vitamin E, far from having pro-oxidative activity, actually increase the anti-oxidative capacity of the liver, especially after ingestion of salmon oil.     

硒和VE对大鼠串珠镰刀菌素毒性的影响

体重７０～８０ｇＷｉｓｔａｒ雄性大鼠５４只随机分成３组，分别饲以低硒低ＶＥ、适硒低ＶＥ和适硒适ＶＥ半合成饲料。４周后每组中的一半动物用串珠镰刀菌素（ＭＦ）２０ｍｇ／（ｋｇ·ｄ）灌胃，另一半用去离子水灌胃作对照。实验持续７周。结果显示：给ＭＦ的动物心肌组织中的硒浓度、琥珀酸脱氢酶、丙酮酸脱氢酶、超氧化物歧化酶、细胞色素Ｃ氧化酶和谷胱甘肽过氧化物酶活力均与对照组无显著差异，但在睾丸组织中硒浓度和谷胱甘肽磷脂氢过氧化物酶活力只分别相当于对照组的５０％和１０％。光镜和电镜检查均未发现ＭＦ会引起心肌病变，但睾丸严重萎缩，造精细胞明显减少。此结果说明ＭＦ的致毒靶器官为睾丸，硒和ＶＥ未显示有保护作用     

Effects of vitamin E on renal dysfunction in chronic cadmium-poisoned rats

Cadmium is a highly toxic metal that can be ingested or inhaled from a variety of industrial and dietary sources. The purpose of this study was to investigate the effects of vitamin E on renal dysfunction and blood pressure changes in chronic cadmium-poisoned rats. Sprague-Dawley rats weighing 100 +/- 10 g were randomly assigned to one control group and three cadmium-poisoned groups. Cadmium groups were assigned to dietary groups according to levels of vitamin E supplementation: vitamin E-free diet (Cd-0E group), 40 mg of vitamin E/kg of diet (Cd-40E group), and 400 mg of vitamin E/kg of diet (Cd-400E group). The animals were raised for 20 weeks, and cadmium was supplied in the drinking water at 50 ppm Cd(2+). The morphological changes observed by both light and electron microscopy revealed mitochondria and tubule epithelial cell edema in the Cd-0E group, yet this was alleviated with the highest level of vitamin E supplementation (Cd-400E group). The urinary beta(2)-microglobulin levels indicated that glomerular injury was higher in the Cd-poisoned groups than in the control group, but were lowered by vitamin E supplementation. Although the glomerular filtration rate (GFR) of the Cd-0E group was significantly lower than that of the control group, the vitamin E-supplemented groups exhibited a similar GFR to the control group, suggesting that vitamin E protected the kidney from functional damage. Angiotensin converting enzyme activity, and blood pressure, and heart rate were all significantly higher in the Cd-poisoned group, but each remained nearly normal with vitamin E supplementation. Accordingly, these results indicate that vitamin E supplementation in chronic cadmium-poisoned rats normalized renal dysfunction and blood pressure regulation.     

Subacute toxicity of paraquat in rats—biochemical effects

The toxic effects of paraquat administered to rats in drinking water for a period of 30 days were studied. Paraquat had no effect on the body weight gain or on organ weights of rats. However, microsomal NADPH-cytochrome c reductase activity and cytochrome P-450 content were increased in rats given paraquat in drinking water. The obtained differences were statistically significant. Serum alkaline phosphatase activity was not significantly changed with respect to control animals but a statistically changed, with respect to control animals, statistically significant decrease was established in serum glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase activity of test animals compared to values obtained for control groups. Hematological data showed that paraquat caused a decrease in hemoglobin concentration and total red blood cell number, while the total white blood cell number was significantly increased compared to values obtained for control animals.     

Effects of dietary fiber on vitamin E status in rats: dose-response to wheat bran

The possible deleterious effects of wheat fiber on vitamin E status were investigated in rats fed semipurified diets supplemented with graded doses (4, 8, 12, 16 or 20%) of Hard Red Spring Wheat Bran, providing 2–10% fiber. After 42 days of experimental feeding, the levels of α-and λ-tocopherol were determined in plasma, liver, pancreas and white adipose tissue (WAT). Total lipids in plasma and total fat excreted in feces were measured. Levels of λ-tocopherol were 5–50 times lower than those of α-tocopherol. Increasing wheat fiber from 2 to 10% in the diet did not significantly decrease levels of vitamers in the four tissues examined. There was a trend towards lower plasma lipid levels with increased percentage fiber in diet. Total fat excretion in feces increased linearly (r²=0.61, P<0.01) between 4 and 10% fiber in diet. When compared to a fiber-free diet, some fiber diets induced lower levels (P<0.05) of α-tocopherol in plasma (4%) and liver (2–6, 10%), but normal diets are not devoid of fiber. It is concluded that addition of wheat fiber to a low or moderate fiber diet has no detrimental effect on vitamin E status in the rat, in spite of increased (+68%, P<0.01) fecal fat excretion     

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)     

Ascorbic and dehydroascorbic acids status in rats fed diets varying in vitamin E levels

Vitamin E, ascorbic and dehydroascorbic acids were determined in plasma and selected tissues of rats fed for 2-3 months different diets varying in vitamin E content. The diets contained as low as 5 IU for group LE, a normal amount of 50 IU for group NE and as high as 250 IU of vitamin E for group HE. Small increases in total vitamin C were observed only in liver, kidney, spleen and plasma with increased dietary levels of vitamin E, however, this was not followed by a substantial increment in the ascorbate/dehydroascorbate ratio. These differences were only observed between diets LE and HE; there was no correlation between vitamin E and vitamin C levels in the tissue. These data suggest that the interactions that readily take place in vitro between these two vitamins do not occur in vivo, probably due to the complexity of natural membranes.     

维生素E与镁对肥胖大鼠糖脂代谢影响的研究

目的观察维生素E(VE)与镁(Mg)对肥胖大鼠糖脂代谢的影响。方法健康Wistar大鼠共74只随机分为5组:正常对照组、高脂高糖组、高脂高糖+VE组、高脂高糖+Mg组和高脂高糖+VE+Mg组。VE和Mg的剂量分别为0.23 g/kg和0.31 g/kg饲料。实验喂养67周处死动物,计算脂肪体重比;检测血脂水平;检测血糖、胰岛素水平,计算胰岛素敏感指数;分析己糖激酶、丙酮酸激酶活性。各结果采用单因素方差分析及析因设计方差分析进行统计。结果高脂高糖组大鼠的体重比正常对照组明显高20%,肥胖大鼠模型建立成功。干预67周后,高脂高糖+VE+Mg组脂体比为13.29%、血浆甘油三酯为0.6 mmol/L,明显低于高脂高糖组的17.24%和1.18 mmol/L(P0.05),且高脂高糖+VE+Mg组甘油三酯水平明显低于高脂高糖+VE组的1.07 mmol/L(P0.05);高脂高糖+VE、高脂高糖+VE+Mg组的己糖激酶活性分别为63.67 U/L和64.61 U/L,较高脂高糖组42.79 U/L和高脂高糖+Mg组44.02 U/L明显增高(P0.05)。结论联合补充VE与Mg可以有效地改善肥胖大鼠脂肪含量及甘油三酯代谢,且降低甘油三酯的作用较单纯补充VE效果显著。此外,其还可以提高肥胖大鼠己糖激酶的活性,且添加VE组较单纯补充Mg组效果更佳。     

Influence of dietary fats and vitamin E on plasma and hepatic vitamin A and beta-carotene levels in rats fed excess beta-carotene

Effects of different dietary lipids and excess vitamin E on plasma and hepatic concentrations of beta-carotene were evaluated in rats fed diets containing a large excess (0.2%) of beta-carotene. Male weanling Wistar Kyoto rats were fed beta-carotene-supplemented diets containing various dietary lipids as follows: Group I, a saturated fat (coconut oil); Group II, a monounsaturated fat (olive oil); Group III, a polyunsaturated fat rich in omega-6 fatty acids (safflower oil); Group IV, same as Group III plus vitamin E; and Group V, a polyunsaturated fat rich in omega-3 fatty acids (menhaden oil). All diets contained 2% safflower oil to provide sufficient amounts of linoleic acid (an essential fatty acid). Rats were killed after six weeks of feeding the various diets, and the concentrations of beta-carotene and vitamin A were determined in plasma and liver. Plasma vitamin A levels were not altered by any of the dietary lipids or by an excess of vitamin E. The concentrations of beta-carotene in plasma were the lowest in rats fed the diet containing menhaden oil. The feeding of the diet containing an excess of vitamin E also resulted in a significant decrease in plasma beta-carotene concentration. Similarly, the hepatic beta-carotene concentration was also reduced to about one-half in rats fed the diet containing an excess of vitamin E. Liver beta-carotene concentration was higher in Groups II and III than in the other three dietary groups. Hepatic vitamin A concentrations were also affected by the type of dietary fat.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased susceptibility to lead toxicity in rats fed semipurified diets

Rats fed stock diets, like Purina Chow, are known to be relatively insensitive to the toxic effects of lead. The addition of lead acetate (1000 ppm of Pb) to the drinking water of 5-week-old rats for 35 days produced toxicity (decreased growth rate and lead-induced anemia) in rats fed semipurified diet, but not in rats fed Purina Rat Chow (Chow). Blood and tissue lead levels also were higher in rats fed semipurified diet than in rats fed Chow. In order to determine whether rats fed semipurified diet could be used as animal models in the determination of permissible levels of lead in the environment, the susceptibility to lead toxicity of these rats to lead-based paints was tested. The addition of 1% paint chips containing 10% lead octoate to the diets resulted in lead toxicity (reduction in growth rates and hematocrit values) only in rats fed the semipurified diet. Rats fed a semipurified diet that permits normal growth are more susceptible to the toxic effects of lead and can be used more effectively in lead toxicity studies than rats fed Chow.     

维生素C和维生素E对糖尿病大鼠非酶糖化和过氧化反应的影响

以链脲佐菌素腹腔注射ＳＤ大鼠建立糖尿病动物模型，在纯营养素饲料配方中补充维生素Ｃ和／或维生素Ｅ，喂饲周，观察单独或联合补充维生素Ｃ、维生素Ｅ对糖尿病非酶糖化及过氧化的干预作用。结果显示维生素Ｃ和Ｅ联合补充可显著减少糖尿病大鼠血红蛋白、低「密度脂蛋白及肾脏皮质的糖化终产物（ＡＧＥｓ）含量，同时显著降低脂质过氧化产物丙二醛（ＭＤＡ）水平，单独补充维生素Ｃ或维生素Ｅ能显著降低糖尿病鼠血清及肾脏ＭＤＡ含量     

Ratio of hemoglobin iron to liver in rats fed different amounts of iron.

Groups of young rats were fed diets containing amounts of iron designed to provide 0.1, 0.3, 1, 3, 10 or 30-times the iron requirement for the rat, and containing two different levels of protein. Iron deficiency anemia was most pronounced in rats receiving the larger amount of protein. In the case of most normal diets, the ratio of iron in the hemoglobin to iron stored in the liver was 26 +/- 6. This is in marked contrast with the ratio of 4.3 found in rats fed a common breakfast cereal.