Pro-carcinogenic activity of beta-carotene, a putative systemic photoprotectant.

Beta-carotene is a strong singlet oxygen quencher and antioxidant. Epidemiologic studies have implied that an above average intake of the carotenoid might reduce cancer risks. Earlier studies found that the carotenoid, when added to commercial closed-formula rodent diets, provided significant photoprotection against UV-carcinogenesis in mice. Clinical intervention trials found that beta-carotene supplementation evoked no change in incidence of nonmelanoma skin cancer. However, when smokers were supplemented with the carotenoid a significant increase in lung cancer resulted. Recently, employing a beta-carotene supplemented semi-defined diet, not only was no photoprotective effect found, but significant exacerbation of UV-carcinogenesis occurred. Earlier, a mechanism, based upon redox potential of interacting antioxidants, was proposed in which beta-carotene participated with vitamins E and C to efficiently repair oxy radicals and, thus, thought to provide photoprotection. In this schema, alpha-tocopherol would first intercept an oxy radical. In terminating the radical-propagating reaction, the tocopherol radical cation is formed which, in turn, is repaired by beta-carotene to form the carotenoid radical cation. This radical is repaired by ascorbic acid (vitamin C). As the carotenoid radical cation is a strongly oxidizing radical, unrepaired it could contribute to the exacerbating effect on UV-carcinogenesis. Thus, vitamin C levels could influence the levels of the pro-oxidant carotenoid radical cation. However, when hairless mice were fed beta-carotene supplemented semi-defined diet with varying levels of vitamin C (0-5590 mg kg(-1) diet) no effect on UV-carcinogenesis was observed. Lowering alpha-tocopherol levels did result in further increase of beta-carotene exacerbation, suggesting beta-carotene and alpha-tocopherol interaction. It was concluded that the non-injurious or protective effect of beta-carotene found in the closed-formula rations might depend on interaction with other dietary factors that are absent in the semi-defined diet. At present, beta-carotene use as a dietary supplement for photoprotection should be approached cautiously.     

Effects of dietary vitamin E supplement on gracile axonal dystrophy (gad) mice

We have studied the effects of dietary vitamin E supplement on the clinical signs and pathological changes in GAD (gracile axonal dystrophy) mice. The control diet contained 2 mg of dl-alpha-tocopheryl acetate (2 I.U.) and vitamin E-supplemented diet contained 58.5 mg of dl-alpha-tocopheryl nicotinate (50 I.U.), per 100 mg of feed. The diet was given to normal (gad/+) and GAD (gad/gad) mice from 21 to 130 days of age. During the feeding, there was no improvement in clinical signs in the GAD mice fed the vitamin E-supplemented diet. The gracile nucleus of the medulla oblongata and the gracile fascicules of the spinal cord were investigated for pathology at 130 days of age, and alpha-tocopherol was also assayed in the serum, liver, brain and spinal cord at that time. There were no pathological differences in the gracile nucleus and fascicules between the GAD mice fed the control and vitamin E-supplemented diet. The alpha-tocopherol levels in the serum and target organs in the control GAD mice were not significantly different from those in control normal mice, showing that GAD mice could absorb and transport alpha-tocopherol. In the supplemented GAD mice, no significant increases in alpha-tocopherol levels were observed in the liver, brain or spinal cord. Particularly, the percentage increase of alpha-tocopherol level in the liver of GAD mice was very low in comparison with that in normal mice, even though the liver can store vitamin E. Thus it may be that the capacity to store vitamin E is lowered in GAD mice. Further studies are needed to investigate in detail the vitamin E metabolism in the mutant mice.     

维生素E对中华鳖幼鳖生长、肝脏维生素E以及血清皮质醇含量的影响

为探讨维生素E(VE)对中华鳖(Pelodiscus sinensis)幼鳖的生长、肝脏VE和血清皮质醇的影响，通过特定生长率、高压液相色谱法和放免法，我们测定了中华鳖幼鳖的生长、肝脏VE和血清皮质醇含量。发现VE添加量为1000和5000mg／kg的两组，能明显降低中华鳖幼鳖的生长。维生素E添加量为500、1000和5000mg／kg的三组，肝脏维生素E含量明显高于对照组，VE添加量在0—1000mg／kg的范围时，肝脏VE的含量随着饲料中VE含量的增加呈指数式增加，并且在VE添加量为5000kg／kg的一组基本达到饱和。维生素E添加量为0和50mg／kg的2组，其血清皮质醇的平均值明显高于维生素E添加量为250、500、1000和5000mg／kg的4组的平均值。上述结果表明：高剂量的VE降低了中华鳖幼鳖的生长和血清皮质醇的含量；在一定剂量范围内，肝脏VE随着饲料中VE含量的增加而升高。     

Vitamin E requirements of juvenile grass shrimp, Penaeus monodon, and effects on non-specific immune responses

A feeding trial was conducted to determine the dietary vitamin E (DL-alpha-tocopheryl acetate, dl-alpha-TOA) requirement and its effect on the non-specific immune responses of juvenile grass shrimp, Penaeus monodon. Purified diets with eight levels (0, 25, 50, 75, 100, 150, 200, 400 mg vitamin E kg diet-1) of supplemental dl-alpha-TOA were fed to P. monodon (mean initial weight 0.29 +/- 0.01 g) for eight weeks. Each diet was fed to three replicate groups of shrimp. Weight gains and total haemocyte count (THC) were higher (P < 0.05) in shrimp fed diets supplemented with 75 and 100 mg vitamin E kg diet-1 than in shrimp fed diets supplemented with 相似文献   

The influence of dietary vitamin C and E supplementation on the physiological response of pirarucu, Arapaima gigas, in net culture

This study evaluated the efficacy of dietary vitamin C (ascorbic acid or AA), vitamin E (alpha-tocopherol or alpha-T), and C+E supplementation on the blood parameters of Arapaima gigas grown in net cages for 45 days. Four treatments were tested: control (commercial feed); C800; E500 and C+E (800+500) with supplementation of 800 mg AA kg(-1), 500 mg alpha-T kg(-1) and 800+500 mg AA+alpha-T kg(-1), respectively. Hematocrit (Ht), red blood cells (RBC), and hemoglobin concentration (Hb) (oxidative status indicators), thrombocytes and leukocytes (immunological indicators), plasma protein and glucose were evaluated. Fish fed vitamin C and C+E supplemented diets showed greater weight gain and survival. Dietary vitamin C and C+E diet supplementation resulted in increased Ht, Hb, RBC, MCHC, total leukocytes, total proteins, thrombocytes and eosinophils compared to the control and alpha-T. The alpha-tocopherol-supplemented diet reduced the number of total thrombocytes, lymphocytes and neutrophils and increased glucose and eosinophils relatively to the control. In general, leukocytes and thrombocytes were good indicators of the efficiency of vitamin on the defense mechanism of the A. gigas reared in cages. Results indicate that high alpha-T diet supplementation provides no benefit for the maintenance of the oxidative or the immunological status of A. gigas. However, it was demonstrated that high dietary AA improves A. gigas immunological status. Red blood cell indices and immune system indicators showed no synergistic effect between the vitamins after supplementing the A. gigas diet with alpha-T+AA.     

Vitamin E supplementation in the mitigation of carbon tetrachloride induced oxidative stress in rats

Oxidative stress is implicated in the pathophysiology of a number of chronic diseases including atherosclerosis, diabetes, cataracts and accelerated aging. The aim of this study was to elucidate the protective role of vitamin E supplementation when oxidative stress is induced by CCl4 administration, using the rat as a model. Rats were fed diets for four weeks either with or without dl-alpha-tocopherol acetate supplementation. Half of the rats (n = 9) from each of the diet groups were then challenged with CCl4 at the completion of the four week diet period. Plasma levels of 8-iso-PGF(2alpha), antioxidant micronutrients and antioxidant enzyme activities were measured to examine changes in oxidative stress subsequent to the supplementation of dl-alpha-tocopherol in the diet. Plasma alpha-tocopherol (vitamin E) concentrations were higher for the groups supplemented with dl-alpha-tocopherol acetate, however the supplemented diet group that was subsequently challenged with CCl4 had significantly lower (p <0.001) plasma alpha-tocopherol concentration than the dl-alpha-tocopherol acetate diet group that was not challenged with CCl4. Total plasma 8-iso-PGF(2alpha) concentration was elevated in diet groups challenged with CCl4, however, the concentration was significantly lower (p <0.001) when the diet was supplemented with dl-alpha-tocopherol acetate. The antioxidant enzymes were not influenced by either dietary alpha-tocopherol manipulation or by the inducement of oxidative stress with CCl4. Plasma concentrations of trans-retinol (vitamin A) were reduced by CCl4 administration in both the dl-alpha-tocopherol acetate supplemented and unsupplemented diet groups. The results of this study indicate that dl-alpha-tocopherol acetate supplementation was protective of lipid peroxidation when oxidative stress is induced by a pro-oxidant challenge such as CCl4.     

Short-term vitamin E intake fails to improve cognitive or psychomotor performance of aged mice

The purpose of this study was to determine if relatively short-term vitamin E supplementation could reverse age-associated impairments in cognitive or motor function and the accumulated oxidative damage in the brain of aged mice. Separate groups of 5- or 20-month-old C57BL6 mice were placed on either a control diet or the same diet supplemented with alpha-tocopheryl acetate (1.65 g/kg). After 4 weeks on the diets, mice were tested for cognitive and motor functions over the next 8 weeks, during which the supplementation was maintained. Vitamin E supplementation increased the concentration of alpha-tocopherol in the cerebral cortex of both the young and old mice, but did not significantly affect oxidative damage to proteins and lipids in the brain cortex. When compared with young controls, the old control mice showed slower learning of a swim maze, longer reaction times, diminished auditory and shock-startle responsiveness, and diminished motor performance on tests of coordinated running and bridge walking. The vitamin E-administered old mice failed to show improvement of function relative to age-matched controls on any of the tests, but did show altered retention performance on the swim maze task and impaired performance in the test of coordinated running. The latter effects were not evident in young mice on the supplemented diet. Results of this study suggest that, when implemented in relatively old mice, supplementation of vitamin E is ineffective in reversing preexisting age-related impairments of cognitive or motor function, and has little effect on common measures of protein or lipid oxidative damage in the mouse brain. Moreover, the current findings indicate that vitamin E could have detrimental effects on some brain functions when implemented in older animals.     

Effects of beta-carotene,vitamin C and E on antioxidant status in hyperlipidemic smokers

Smoking can accelerate the consumption of the stored antioxidant vitamins and increase the oxidative stress in the hyperlipidemic patients. The study investigated the effects of combined beta-carotene, vitamin C, and vitamin E on plasma antioxidant levels, erythrocyte antioxidative enzyme activities, and LDL lipid peroxides. Male hyperlipidemic smokers (35-78 years old) were randomly divided into two antioxidant supplemented groups: intervention 1 (I1, n = 22) (15 mg beta-carotene/day, 500 mg vitamin C/day, and 400 mg alpha-tocopherol equivalent/day) and intervention 2 (I2, n = 20) (30 mg beta-carotene/day, 1000 mg vitamin C/day, and 800 mg alpha-tocopherol equivalent/day). After 6-week supplementation, plasma beta-carotene, vitamin C, vitamin E, and erythrocyte glutathione levels increased significantly by 200%, 98%, 129%, and 39%, respectively, in the I1 group, and by 209%, 216%, 197%, and 32%, respectively, in the I2 group. Plasma Fe(+2) concentrations and Fe(+2)/Fe(+3) decreased significantly in both groups. Except erythrocyte glutathione peroxidase activity in the I1 group, erythrocyte catalase, glutathione peroxidase, and superoxide dismutase activities increased significantly in both groups. Lipid peroxides in LDL decreased significantly by 56% and 72% in the I1 and I2 groups, respectively. However, the levels of plasma iron, erythrocyte glutathione, and LDL lipid peroxides, and the activities of erythrocyte antioxidative enzymes did not differ between two groups. In conclusion, combined antioxidant supplements increased plasma antioxidant levels and antioxidative enzyme activities, and lowered LDL lipid peroxides in male hyperlipidemic smokers. Higher dosage of the supplements did not have an additive effect.     

Dietary vitamin E supplementation affects tissue lipid peroxidation of hybrid tilapia,Oreochromis niloticus x O. aureus

A feeding trial was conducted to evaluate the effects of dietary vitamin E contents on the growth, ascorbate induced iron-catalyzed lipid peroxidation in post-mortem muscle and liver tissue, and Raman spectral changes in lens of juvenile hybrid tilapia (Oreochromis niloticus x O. aureus). Experimental fish were fed practical diets supplemented with 0, 50, 100, 200, 450 and 700 mg alpha-tocopheryl acetate/kg diet for 14 weeks. There was no significant difference in weight gain, feed conversion ratio and protein efficiency ratio among fish fed test diets (P>0.05). Protein content of fish fed diet containing the lowest vitamin E level was the lowest (P<0.05) among all groups. No difference was found in other body constituents among test fish (P>0.05). The thiobarbituric acid-reactive substances produced by iron-catalyzed lipid peroxidation in muscle and liver tissue of fish fed the diet without alpha-tocopheryl acetate supplementation were significantly (P<0.05) greater than those from fish fed diets containing higher levels of alpha-tocopheryl acetate. Dietary vitamin E supplementation increased the antioxidant capability of tilapia tissues against lipid peroxidation. Further, dietary vitamin E supplementation also influenced the lens cortical membrane structure of tilapia.     

Influence of vitamin E on gastric mucosal injury induced by Helicobacter pylori infection

We investigated the effect of vitamin E on gastric mucosal injury induced by Helicobacter pylori (H. pylori) infection. Male Mongolian gerbils were divided into 4 groups (normal group without H. pylori infection, vitamin E-deficient, -sufficient and -supplemented groups with H. pylori infection). Following oral inoculation with H. pylori (ATCC43504 2 x 10(8) CFU), animals were fed diets alpha-tocopherol 2 mg/100 g diet in the normal and vitamin E-sufficient groups and alpha-tocopherol 0.1 mg/100 g and 50 mg/100 g in the vitamin E-deficient and -supplemented groups, respectively, for 24 weeks. Chronic gastritis was detected in all gerbils inoculated H. pylori. Gastric ulcer was detected in 2 of 7 gerbils only in the vitamin E-deficient group. In the vitamin E-deficient group, myeloperoxidase activity and mouse keratinocyte derived chemokine (KC) in gastric mucosa was significantly higher than in the vitamin E supplemented group. Subsequently, in an in vitro study expression of CD11b/CD18 on neutrophils was enhanced by H. pylori water extract. This effect was suppressed in a dose dependent manner by the addition of alpha-tocopherol. These results suggest that vitamin E has a protective effect on gastric mucosal injury induced by H. pylori infection in gerbils, through the inhibition of accumulation of activated neutrophils.     

The effect of vitamin E on lipid peroxidation in the copper-deficient rat

The present study was designed to determine whether the supplementation of vitamin E in the copper-deficient diet would ameliorate the severity of copper deficiency in fructose-fed rats. Lipid peroxidation was measured in the livers and hearts of rats fed a copper-deficient diet (0.6 microg Cu/g) containing 62% fructose with adequate vitamin E (0.1 g/kg diet) or supplemented with vitamin E (1.0 g/kg diet). Hepatic lipid peroxidation was significantly reduced by vitamin E supplementation compared with the unsupplemented adequate rats. In contrast, myocardial lipid peroxidation was unaffected by the level of vitamin E. Regardless of vitamin E supplementation, all copper-deficient rats exhibited severe signs of copper deficiency, and some of the vitamin E-supplemented rats died of this deficiency. These findings suggest that although vitamin E provided protection against peroxidation in the liver, it did not protect the animals against the severity of copper deficiency induced by fructose consumption.     

Effects of vitamin C and vitamin E on lipid peroxidation, blood serum metabolites, and mineral concentrations of laying hens reared at high ambient temperature

This study was conducted to determine the effects of vitamin C (L-ascorbic acid) and vitamin E (alpha-tocopherol acetate) on serum concentrations of lipid peroxidation (MDA) and triiodothyronine (T3), thyroxine (T4), adrenocorticotropic hormone (ACTH), and some metabolite and mineral in laying hens reared at high ambient temperatures ranging from 25 degrees C to 35 degrees C. One hundred twenty laying hens (18 wk old; Hy-Line) were divided into 4 groups, 30 hens per group. The laying hens were fed either a basal diet (control) or the basal diet supplemented with either 250 mg of L-ascorbic acid/kg of diet (vitamin C), 250 mg of alpha-tocopherol acetate/kg of diet (vitamin E), or 250 mg of L-ascorbic acid plus 250 mg alpha-tocopherol acetate/kg of diet (combination). Separately or as a combination vitamins C and E increased serum vitamin C and vitamin E concentrations (p < 0.001) but decreased serum MDA concentration (p < 0.05). Serum concentrations of vitamin E and vitamin C were found highest but serum MDA concentration was lowest in the combination group. Supplemental vitamins C and E either separately or in a combination increased serum T3 and T4 concentrations (p < 0.05), whereas decreased serum ACTH concentration (p < 0.01). Serum glucose and cholesterol concentrations decreased, whereas serum protein concentration increased (p < 0.05) when vitamins C and E singly or together were added to the diet. Vitamin C and vitamin E supplementation resulted in an increase in serum concentrations of Ca, P, and K (p < 0.01) but a decrease in serum concentration of Na (p < 0.05). The results of the present study suggest that supplemental vitamin C and vitamin E alter serum lipid peroxidation, vitamin C, vitamin E and metabolite status, and diets supplemented with a combination of these two vitamins offer a good management practice in laying hens reared at high temperatures. In addition, the results suggest that dietary vitamin C and vitamin E act synergistically.     

High dietary intake of alpha-tocopherol acetate enhances the non-specific immune response of gilthead seabream (Sparus aurata L.)

To determine the effects of three high levels of dietary intake of alpha-tocopherol acetate (vitamin E) on the non-specific immune response of gilthead seabream (Sparus aurata L.), specimens were fed a commercial diet (100 mg alpha-tocopherol kg-1) as control, or vitamin E supplemented diets (600, 1200 or 1800 mg alpha-tocopherol acetate kg-1) for 15, 30 or 45 days. Growth, serum alpha-tocopherol levels, natural haemolytic complement activity and head-kidney leucocyte migratory, respiratory burst and phagocytic activities were studied at each of the assay times. A positive correlation between alpha-tocopherol acetate intake and serum alpha-tocopherol levels was observed, the increase being linked to both the dosage and length of treatment. Specimens fed the diet supplemented with 600 mg vitamin E kg-1 showed no enhancement in any of their immune parameters, while those fed the diet supplemented with 1200 mg vitamin E kg-1 presented a slightly higher (but not statistically significant) specific growth rate than fish fed the other diets. In addition, serum haemolytic activity and the phagocytosis of head-kidney leucocytes were enhanced by the dietary intake of 1200 mg vitamin E kg-1 after 30 and 45 days of treatment, although leucocyte migration and respiratory burst activity remained unaffected. The highest vitamin E dietary dose used, 1800 mg kg-1, unexpectedly provoked no immunostimulation. These results indicate that a moderate level of vitamin E in the diet (1200 mg kg-1) stimulates the seabream's non-specific immune system after 30 days of administration. Lower or higher vitamin E concentrations may not be so effective, because of an imbalance in the vitamin E ratio with other antioxidants. The proposed dietary levels of vitamin together with the indicated administration time could be useful for reducing the susceptibility of farmed fish to infectious diseases.     

Parameters of dietary selenium and vitamin E deficiency in growing rabbits.

4 x 5 growing female rabbits (New Zealand White) with an initial live weight of 610 +/- 62 g were fed a torula yeast based semisynthetic diet low in selenium (<0.03 mg/kg diet) and containing <2 mg alpha-tocopherol per kg (group I). Group II received a vitamin E supplementation of 150 mg alpha-tocopherylacetate per kg diet, whereas for group III 0.40 mg Se as Na-selenite and for group IV both supplements were added. Selenium status and parameters of tissue damage were analyzed after 10 weeks on experiment (live weight 2,355 +/- 145 g). Selenium depletion of the Se deficient rabbits (groups I and II) was indicated by a significantly lower plasma Se content (group I: 38.3 +/- 6.23 microg Se/mL plasma, group II: 42.6 +/- 9.77, group III: 149 +/- 33.4, group IV: 126 +/- 6.45) and a significantly lower liver Se content (group I: 89.4 +/- 18.2 microg/kg fresh matter, group II: 111 +/- 26.2) as compared to the Se supplemented groups III (983 +/- 204) and IV (926 +/- 73.9). After 5 weeks on the experimental diets differences in the development of plasma glutathione peroxidase were observed. As compared to the initial status group (45.2 +/- 4.50) pGPx activity in mU/mg protein was decreased in group I (19.1 +/- 7.08), remained almost stable in the vitamin E supplemented group II (46.3 +/- 11.2) whereas an elevated enzyme activity was measured in the Se supplemented groups III (62.4 +/- 23.9) and IV (106 +/- 19.9). In the rabbit organs investigated 10 weeks of Se deficiency caused a significant loss of Se dependent cellular glutathione peroxidase activity (GPx1) of 94% (liver), 80% (kidney), 50% (heart muscle) and 60% (musculus longissimus dorsi) in comparison to Se supplemented control animals. Damage of cellular lipids and proteins in the liver was due to either Se or vitamin E deficiency. However damage was most severe under conditions of a combined Se and vitamin E deficiency. It can be concluded that the activity of plasma glutathione peroxidase is a sensitive indicator of Se deficiency in rabbits. The loss of GPx1 activity indicates the selenium depletion in various rabbit organs. Both selenium and vitamin E are essential and highly efficient antioxidants which protect rabbits against lipid and protein oxidation.     

Effect of oat by-product antioxidants and vitamin E on the oxidative stability of pork from pigs fed diets supplemented with linseed oil

The aim of the experiment was to compare the antioxidative potential of an oat by-product with the effect of vitamin E on the oxidative stability of pork from pigs fed a diet enriched with linseed oil. Thirty-four crossbreed barrows were fed individually from 39 to 109 kg body weight (BW) on one of four diets: a control diet based on barley-triticale-soybean (Diet C), a diet containing an oat byproduct (Diet O), and the same diets supplemented with vitamin E (100 mg/kg diet) (Diets CE and OE, respectively). The oat by-product, comprising oat hulls and bran, was included at 10 and 20% in the grower and finisher diets, respectively. To Diets O and OE, refined rapeseed oil was added to equalise their energy content to Diets C and CE. Compared to Diets C and CE, the inclusion of the oat by-product in Diets O and OE increased the antioxidative capacity of water-soluble and lipid soluble compounds in these diets. Dietary treatment did not influence growth performance, slaughter value, longissimus dorsi (LD) muscle quality measured by nutrient contents, pH, drip loss or colour. Vitamin E supplementation increased the alpha-tocopherol concentration in serum and meat (p < 0.01), and decreased the formation of thiobarbituric acid reactive substances (TBARS) in the fresh and stored LD (p < 0.01). In addition, diets with the oat by-product increased serum alpha-tocopherol concentration (p < 0.01) and decreased the TBARS levels in the fresh and stored LD (p < 0.05), without increasing muscle alpha-tocopherol concentration. The obtained results indicate that the phenolic compounds present in oat by-products have a considerable antioxidant potential and a beneficial effect on the pig organism and oxidative stability of meat. However, dietary inclusion with the oat by-product was not as efficient as supplementation with vitamin E.     

Influence of dietary vitamin E and C supplementation on vitamin E and C content and thiobarbituric acid reactive substances (TBARS) in different tissues of growing pigs

To investigate the influence and possible interactions of dietary vitamin E and C supplementation on vitamin content of both vitamins and oxidative stability of different pork tissues 40 Large White barrows from 25 kg to 106 kg were allocated to four different cereal based diets: Basal diet (B), dl-alpha-tocopherylacetate + 200 mg/kg (E), crystalline ascorbic acid + 300 mg/kg (C) or both vitamins (EC). At slaughtering samples of liver, spleen, heart, kidney, backfat outer layer, ham and M. tongissimus dorsi were obtained. Growth performance of the pigs and carcass characteristics were not influenced by feeding treatments. Dietary vitamin E supplementation had a significant effect on the vitamin E and alpha-tocopherol concentration in all investigated tissues. Backfat outer layer, liver, spleen, kidney and heart had higher vitamin E concentrations than ham and M. longissimus dorsi. Dietary vitamin C supplementation tended towards enhanced vitamin E levels except for ham samples. Therefore, some synergistic actions without dietary vitamin E supplementation between the two vitamins could be shown. The vitamin C concentration and TBARS were increased or at least equal in all tissues due to vitamin C supplementation. Dietary alpha-tocopherol supplementation resulted in lower TBARS in backfat outer layer (malondialdehyde 0.35 mg/kg in B vs. 0.28 mg/kg in E), but increased in heart and ham. When both vitamins were supplemented (EC) TBARS were lower in M. longissimus dorsi and backfat outer layer, equal in heart and higher in liver and ham compared to a single vitamin C supplementation. Rancimat induction time of backfat outer layer was 0.3 h higher in C compared to B and 0.17 h higher in EC than in E. Correlations between levels of both vitamins were positive for kidney (r = 0.169), M. longissimus dorsi (r = 0.499) and ham (r = 0.361) and negative for heart (r = -0.350). In liver and spleen no interaction could be found. In backfat outer layer vitamin E was positively correlated with rancimat induction time (r = 0.550) and negatively with TBARS (r = -0.202), but provided no evidence that dietary vitamin E supply led to better oxidative stability.     

Dietary fatty acid composition rather than vitamin E supplementation influence ex vivo cytokine and eicosanoid response of porcine alveolar macrophages

This study examined the influence of different dietary fat sources (animal fat, sunflower oil, and fish oil) and supplementation of vitamin E (85, 150 and 300 mg all-rac-alpha-tocopheryl acetate/kg diet) on the ex vivo synthesis of eicosanoids and cytokines by porcine alveolar macrophages. Supplementation of vitamin E provoked an increase in the concentration of alpha-tocopherol of the macrophages irrespective of fat sources. Fish oil increased the macrophage n-3 content with 100% and 40%, and reduced the n-6 with 60% and 53% in comparison with sunflower oil and animal fat, respectively. Fish oil decreased the production of TNF-alpha, IL-8, LTB4, and PGE2 (but not IL-6) relative to the other dietary fat sources, and no difference was observed between sunflower oil and animal fat. Positive correlations were found between the n-6 fatty acid content and the production of PGE2, and the PGE2 production was positively correlated with TNF-alpha and IL-8. Negative correlations were found between the n-3 PUFA content and the concentration of PGE2, TNF-alpha and IL-8. In conclusion, dietary fish oil supplemented at a level of 5%, but not supplemental vitamin E, influenced the inflammatory responses of alveolar macrophages isolated from weaned pigs relatively to animal fat and sunflower oil.     

Vitamin E and beta-carotene status of dairy cows: a survey of plasma levels and supplementation practices

Culling rate in dairy cattle has increased considerably, thereby reducing cowś longevity and raising sustainability concerns worldwide. In the last decades, feeding systems have changed towards larger inclusion of preserved forages and reduced fresh herbage, which may limit vitamin E and beta-carotene dietary supply to dairy cows. Because of higher oxidative stress, engendered by greater milk production of modern genetics, the requirement for these nutrients is increased. Therefore, this study aimed to assess the current status of vitamin E and beta-carotene of commercial dairy cows. Blood vitamin E and beta-carotene concentrations were measured in 2 467 dairy cows from 127 farms in Belgium, Germany, Iberia and The Netherlands, that were visited once. Five cows were randomly selected per lactation stage per farm: Dry (between 30 and 1 day(s) before calving), Very-early (from calving until 15 days in milk (DIM)), Early (between 16 and 119 DIM), and Mid-late (from 120 DIM onwards). In addition, a survey was conducted to retrieve data on vitamin E and beta-carotene supplementation and feeding practices. Vitamin E and beta-carotene blood concentrations dropped considerably around calving. Among all surveyed cows, more than 75 and 44% were deficient in vitamin E and beta-carotene (i.e., blood concentration below 3.0 and 3.5 mg/l, respectively). Of the Very-early group, more than 97 and 78% of the cows were deficient in vitamin E and beta-carotene, respectively, with respective blood concentrations of 1.15 and 2.71 mg/l, which was significantly lower than the other lactation stages. Vitamin E and beta-carotene blood concentrations, as well as their supplementation levels, significantly varied among countries. Vitamin E and beta-carotene blood concentrations were positively related to the total estimated daily intakes of vitamin E and beta-carotene. Therefore, blood concentrations of vitamin E and beta-carotene depend on their respective level of intake, which is generally below recommendations and varies greatly between countries. Supplementation could contribute to provide cows with adequate amounts of vitamin E and beta-carotene all along the lactation, to ensure their lifetime performance and improve their fertility.     

Influence of vitamins A, D3 and E status on post-mortem meat quality in steers under winter housing or pasture finishing systems

We investigated the influence of Swedish recommended vitamins A, D3 and E supplementation levels on muscle tenderness and fatty acid (FA) composition under indoor or outdoor finishing programmes. Swedish Red breed steer calves were divided into vitamin supplemented (n = 12) and non-supplemented (n = 15) groups while on pasture prior to the finishing period. This trial began at the beginning of the winter housing period during which the steers were fed a 55 : 45 dry matter barley : grass silage diet indoors. The indoor finished group was comprised of vitamin supplemented (n = 6) and non-supplemented (n = 8) steers slaughtered after about 155 days on feed. Vitamin supplemented steers were provided with 100 g mineral supplement providing 400 000 IU vitamin A, 100 000 IU D3 and 3000 IU E daily as recommended for Swedish production practices. In spring, outdoor finished vitamin supplemented (n = 6) and non-supplemented (n = 7) steers grazed semi-natural grassland for an additional 120 days before slaughter. During pasture, vitamin supplemented steers had free-choice access to a mineral supplement containing vitamins A, D3 and E. The mineral supplement for the non-supplemented steers did not contain vitamins A, D3 and E and was provided at the same amount as the vitamin supplemented steers. Shear force values were similar between vitamin supplemented and non-supplemented steers after ageing 2, 7 and 14 days within indoor and outdoor finishing programmes. The shear force values had decreased by 14 days of ageing within all programmes. The μ- and m-calpain activity did not differ between vitamin supplemented and non-supplemented steers for either the indoor or outdoor finishing programmes. The calpastatin activity was higher for the indoor, vitamin supplemented steers. Indoor finished vitamin supplemented steers had a greater proportion of C18:1c-9 and total monounsaturated fatty acids, whereas the non-supplemented steers had a greater proportion of total saturated fatty acids. We concluded that the meat quality from steers not receiving vitamin supplementation was similar to that of steers receiving vitamins A, D3 and E supplementation at Swedish recommended levels under indoor and outdoor finishing programmes.     

Influence of dietary vitamin E on prostaglandin biosynthesis in rat blood.

A vitamin E (alpha-tocopherol) deficient diet stimulated prostaglandin biosynthesis in coagulating rat blood. Prostaglandins were extracted from serum, purified and bioassayed. The identity of prostaglandin E2 was confirmed by gas chromatography-mass spectrometry. Withholding vitamin E from the diet caused a marked increase in PGE2 and a lesser increase in PGF2alpha production in serum. In rats maintained on diets containing different concentrations of vitamin E, serum concentrations of PGE2 and PGF2alpha were inversely related to serum concentrations of alpha-tocopherol. These data suggest that in vitro alpha-tocopherol inhibits the endogenous conversion of arachidonic acid into PGE2 and PGF2alpha. The possibility that alpha-tocopherol may inhibit the formation of endoperoxide intermediates of PGE2 and PGF2alpha biosynthesis and subsequent induction of platelet aggregation is discussed.