Vitamin E-supplemented Diet Research Articles

Effect of dietary vitamin E on oxidative stress-related gene-mediated differences in anxiety-like behavior in inbred strains of mice

It has been reported that the degree of anxiety-like behavior differs between inbred strains of mice, and that this phenomenon was linked to the expression levels of the oxidative stress-related genes glyoxalase 1 (Glo1) and glutathione reductase 1 (Gsr) in the brain. Therefore, we investigated whether antioxidative activity in the brain affects the Glo1 and Gsr mRNA expressions and strain-dependent anxiety-like behavior using mice fed different amounts of vitamin E. First, we measured brain Glo1 and Gsr mRNA levels and evaluated the anxiety-like behaviors presented by C57BL/6J (B6) and DBA/2C (D2) mice. We demonstrated that D2 mice presented both significantly elevated Glo1 and Gsr mRNA levels as well as more prominent anxiety-like behavior in elevated plus-maze and open field tests. Next, we fed mice from these two strains either a control, vitamin E-free, or vitamin E-supplemented diet for four weeks. Plasma, liver, and brain α-tocopherol concentrations changed in a dose-dependent manner. However, neither brain Glo1 and Gsr mRNA levels nor anxiety-like behavior were affected by dietary vitamin E intake. These results demonstrated that while strain-dependent anxiety-like behavior in mice was related to oxidative stress-related gene expression, the regulatory mechanisms for these genes and anxiety-like behaviors were independent of antioxidative activity in the brain. Strain-dependent differences of the anxiety in mice are probably related to the anxiolytic effects of methylglyoxal, a substrate for Glo1 and Gsr.

Protective effect of dietary vitamin E on immunological and biochemical induction through silver nanoparticles (AgNPs) inclusion in diet and silver salt (AgNO3) exposure on Zebrafish (Danio rerio)

The present study evaluated silver nanoparticle (AgNPs) toxicity using biomarkers of oxidative and metabolic stress, immunological impairment and cellular damage in zebrafish (Danio rerio), as well as the optimal dose of vitamin E neutralizing undesirable effects. Fish were fed for ten days and eight study groups were investigated: controls, AgNPs exposure alone (1.5 mg L−1) and combined with three different vitamin E doses (1.5 mg L−1 of AgNPs + vitamin E 100, 200 or 400 mg kg−1 of food), also one positive control group exposed to AgNO3 alone or combined with the same vitamin E doses. D. rerio exposed to AgNPs alone or combined with the lower vitamin E dose showed overall worse results in comparison with the control groups and the groups combining nanoparticles and 200 or 400 mg kg−1 of food of vitamin E-supplemented diet. AgNPs caused cell impairment by increasing LDH activity and cortisol levels, generated oxidative stress by inhibiting SOD and CAT activity and immunosuppression by inhibiting ACH50 and lysozyme activity. The groups exposed to Ag salt showed the same response-pattern found for the NPs groups, reinforcing that Ag toxicity of AgNPs is mediated by Ag+. In conclusion, although AgNPs are toxic to Danio rerio, vitamin E supplementation at 200 or 400 mg kg−1 can act protectively against its toxic effects.

The protective role of vitamin E on Oreochromis niloticus exposed to ZnONP

The present study evaluated if ZnONPs induce oxidative stress, immunological impairment and cellular damage in tilapia (Oreochromis niloticus), as well as the possible protective effect of vitamin E. Fish were fed for ten days and five study groups were investigated: controls, two ZnONPs concentrations (1.5 and 2.5mgL−1) and 1.5 and 2.5mgL−1 of ZnONPs + vitamin E (500mgkg−1 of food). O. niloticus treated with ZnONPs, showed decreased health in comparison with the control group and the groups that combined nanoparticles and vitamin E-supplemented diet. ZnONPs caused cell impairment by increasing ALT, AST and ALP activity and generated oxidative stress by inhibiting SOD and CAT activity. Biochemical changes of these biomarkers were prevented by vitamin E, although this compound did not confer complete protection. In conclusion, ZnONPs are toxic to O. niloticus, affecting antioxidant defenses, with vitamin E acting protectively against this toxic effect.

Effects of dietary vitamin E and selenium nanoparticles supplementation on acute stress responses in rainbow trout (Oncorhynchusmykiss) previously subjected to chronic stress

The aim of the present study was to evaluate the effects of dietary vitamin E, nanoselenium (nanoSe), and their combination on growth and acute stress responses in rainbow trout previously subjected to chronic stress. The fish were divided into five groups according to stocking density and diet: Normal (20kgm−3; basal diet), Dense (80kgm−3; basal diet), Vit E (80kgm−3; 500mgkg−1 vitamin E-supplemented diet), NanoSe (80kgm−3; 1mgkg−1 nanoSe-supplemented diet), and Combination (80kgm−3; 500mgkg−1 vitamin E and 1mgkg−1 nanoSe-supplemented diet). The fish in each group were weighed after 60days. The best growth under high density condition was observed in fish fed on vitamin E-supplemented diets (Vit E and Combination groups). Following high stocking rearing, fish were subjected to an acute confinement stress by decreasing water volume in the tanks (200kgfishm−3) for 45min and sampled at 0, 2, 4, 8 and 24h post-stress to evaluate the fish performance to additional stressors. The levels of serum cortisol, glucose, lactate, alanine aminotransferase, aspartate transaminase, and alkaline phosphatase were significantly higher in the Dense group at most of time points after initiation of acute stress. The results showed that rainbow trout can reach adaptation to chronic stress conditions, resulting in intensified stress responses to an acute stressor. The data also showed that vitamin E-supplemented diets can exert positive effects on the welfare of chronically stressed rainbow trout subjected to an additional acute stressor.

The protective effect of vitamin E against changes in fatty acid composition of phospholipid subclasses in gill tissue of Oreochromis niloticus exposed to deltamethrin

The effects of deltamethrin on the fatty acid composition of phospholipid subclasses (phosphatidylchlonine (PC), phosphatidylethanolamine (PE), phosphatidylinositole (PI) and phosphatidylserine (PS)) in gill tissue of Oreochromis niloticus (Perciformes: Cichlidae) and the possible protective effect of vitamin E against deltamethrin were determined by gas chromatography. The changes in the fatty acid profile were analysed after 14 d of exposure. Treatments included Group I (fed with basal diet only), Group II (fed with vitamin E-supplemented diet), Group III (fed with basal diet and exposed to deltamethrin) and Group IV (fed with vitamin E-supplemented diet and exposed to deltamethrin). The effects of deltamethrin on PI, PE and PS were valid for the total saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs). The effect on PC was detected in total SFAs and total PUFAs. The vitamin E-supplemented diet did not show complete protective effect on fatty acid composition of the fish exposed to deltamethrin. However, the protective effect was observed in total SFAs, total MUFAs and total PUFAs in PC. In PI, protective effect was only recorded on total PUFAs. There was no protective effect in PS and PE. The results of the present study demonstrated that deltametrin exposure had harmful effects on cell membrane and treatment with vitamin E could only partially protect fish gills.

Effect of Dietary Vitamin E Supplementation on Liver Oxidative Damage in Rats with Water-Immersion Restraint Stress.

We examined how dietary supplementation of vitamin E protects against liver oxidative damage in rats with water-immersion restraint stress (WIRS). Before WIRS exposure, rats received a normal diet (ND) or vitamin E-supplemented diet (VESD) (500 IU α-tocopherol/kg diet) at a mean dose of 15 g/animal/d for 4 wk. The two diet groups had serum transaminases and lactate dehydrogenase activities and adrenocorticotropic hormone, corticosterone, and glucose levels to a similar extent. VESD-fed rats had higher liver α-tocopherol concentrations and lower liver ascorbic acid, total coenzyme Q9 (CoQ9), reduced CoQ9, reduced CoQ10, and lipid peroxide (LPO) concentrations than ND-fed rats. When the two diet groups were exposed to 6 h of WIRS, the serum liver cell damage index enzyme activities increased more greatly in ND-fed rats than in VESD-fed rats but the serum stress marker levels increased to a similar extent. The WIRS exposure caused no change in liver LPO concentration with the further increase in liver α-tocopherol concentration in VESD-fed rats but increased liver LPO concentration without changing liver α-tocopherol concentration in ND-fed rats. Upon the WIRS exposure, liver reduced glutathione concentration decreased with the further decrease in liver ascorbic acid concentration in VESD-fed rats and those concentrations decreased in ND-fed rats. The WIRS exposure recovered the decreased liver total CoQ9 and reduced CoQ9 concentrations in VESD-fed rats but decreased liver total CoQ9, reduced CoQ9, and reduced CoQ10 concentrations in ND-fed rats. These results indicate that dietary vitamin E supplementation protects against liver oxidative damage without affecting the stress response in rats with WIRS.

Effect of vitamin E on alloxan-induced mouse diabetes

ObjectivesAlloxan generates hydrogen peroxide in the body, and a small amount of alloxan administered to acatalasemic mice results in diabetes. D-α-Tocopherol (vitamin E) is an antioxidant which helps prevent excess oxidation in the body. In this study, we examined the effect of vitamin E on diabetes caused by alloxan administration in mice. MethodsMice were maintained on a vitamin E-deprived diet and supplemented diet, respectively, for 14weeks. Alloxan was then intraperitoneally administered, and blood glucose, glucose tolerance and the insulin level in mouse blood were examined. ResultsHyperglycemia was observed in the mice maintained on the vitamin E-deprived diet. The incidence of hyperglycemia in the mice maintained on the vitamin E-deprived diet was significantly higher than that in the mice maintained on the supplemented diet. The abnormal glucose metabolism caused by alloxan administration was ameliorated by the vitamin E-supplemented diet. ConclusionsIt is deduced that vitamin E can prevent a decrease of insulin concentration in the blood in this mouse model.

The protective role of vitamin E on the fatty acid composition of phospholipid structure in gill and liver tissues of Oreochromis niloticus exposed to deltamethrin

Deltamethrin is a commonly used pyrethroid pesticide. Vitamin E is a antioxidant that plays an important role in protecting cells against toxicity by inactivating free radicals generated following pesticides exposure. Therefore, in the present study, it was evaluated whether deltamethrin induced changes on the fatty acid composition of phospholipid in gill and liver tissues in Oreochromis niloticus and, the possible protective effect of vitamin E against deltamethrin was determined. Fish was fed with no pesticide+control diet, no pesticide+vitamin E-supplemented diet, 1.45μg/l deltamethrin+control diet, 1.45μg/l deltamethrin+vitamin E-supplemented diet for twenty days. Pesticide and diet quality made an impact on the fatty acid composition of phospholipid. In treatments of deltamethrin, group fed with control diet showed much greater damage in comparison with group fed with vitamin E supplemented diet. The results indicated that the deltamethrin led to an increase in the percentages of total SFAs (saturated fatty acids) and total MUFAs (monounsaturated fatty acids) and a decrease in total PUFAs (polyunsaturated fatty acids) in the gill tissues. However, coadministration of deltamethrin and vitamin E showed decrease in the percentages of saturated fatty acids and increase in the percentages of polyunsaturated fatty acids in the gill tissues. In group fed with control diet, deltamethrin led to a decrease in the percentage of SFAs and a increase in total MUFAs in the liver. Coadministration of deltamethrin and vitamin E showed increase in the percentages of polyunsaturated fatty acids in the liver tissues. These results have demonstrated that administration of vitamin E along with deltamethrin decreases the peroxidation of unsaturated fatty acids and thus protects the cell membranes.

The protective role of vitamin E on gill and liver tissue histopathology and micronucleus frequencies in peripheral erythrocytes of Oreochromis niloticus exposed to deltamethrin

Deltamethrin, is a commonly used pyrethroid pesticide. Vitamin E is a antioxidant that plays an important role in protecting cells against toxicity by inactivating free radicals generated following pesticides exposure. Therefore, it was evaluated whether deltamethrin induced histopathological changes and nuclear abnormalities using micronucleus test in Oreochromis niloticus, and the possible protective effect of vitamin E against deltamethrin inducing adverse effects in O. niloticus were investigated. Fish was fed with no pesticide+control diet, no pesticide+vitamin E-supplemented diet, 1.45μg/l deltamethrin+control diet, 1.45μg/l deltamethrin+vitamin E-supplemented diet for 30 days. Pesticide and diet quality made an impact on histopathological lesions. In treatments of deltamethrin, group fed with control diet showed much greater damage in comparison with group fed with vitamin E supplemented diet. Vitamin E decreased some histopathological changes induced by deltamethrin, but did not confer complete protection. Deltamethrin treatment has been shown to results in a significant increase in the frequency of micronucleus. However, coadministration of deltamethrin and vitamin E showed decrease in the frequency of micronucleus as compared to deltamethrin treated fish. Our results indicate that, the MN assay and histopathology can be used as bioassays for monitoring pollution in aquatic medium. On the other hand, it was observed that vitamin E decreased the genotoxicity and histopathological changes induced by deltamethrin.

Effects of pregnenolone-16α-carbonitrile on vitamin E status and protein levels of antioxidant enzymes in male rats fed a vitamin E-supplemented diet

The aim of this study was to evaluate the effects of the administration of pregnenolone-16α-carbonitrile (PCN), an inducer of the cytochrome P450 3A gene in rats, on vitamin E status and antioxidant enzyme protein levels in rats fed a vitamin E-supplemented diet. Two groups of male Wistar rats were fed for 3 weeks with a basal diet containing 50 ppm of α-tocopherol or the same diet containing 10 times more α-tocopherol. In the final 3 days, each group was divided into two subgroups which were given a single daily intraperitoneal injection of PCN at 75 mg/kg (groups PCN and PCN+VE) or DMSO (groups DS and DS+VE). PCN treatment alone significantly reduced the α-tocopherol content of the liver and plasma and this effect was prevented by supplementation with 10-fold more α-tocopherol. α-Tocopherol levels in the kidneys, lung, heart, and testes were significantly higher in both vitamin E-supplemented groups than in the control groups. TBARS levels in the liver and lung were significantly increased in both PCN-treated groups, as shown by two-way ANOVA analysis. PCN also caused a significant reduction in protein levels of catalase and glutathione peroxidase (GPx) in both groups. Dietary vitamin E supplementation caused a decrease in liver protein levels of GPx and superoxide dismutase, but not catalase, in both groups and protected against PCN-induced lipid peroxidation, which was caused by CYP3A induction and a reduction in antioxidant enzyme levels.

Effect of Vitamin E on Learning and Memory Deficit in Aged Rats

In order to verify whether vitamin E improves the cognitive impairment induced through aging, aged rats fed a vitamin E-supplemented diet had their learning and memory functions assessed in comparison with the aged rats fed a normal diet using a Morris water maze test. Although normal aged rats showed very poor learning ability concerning the place of a platform in the water maze apparatus, the aged rats fed the vitamin E-supplemented diet learned the place with a marked speed in only 5 trials. After old animals showed the maximum learning ability, they were kept in a normal atmosphere for 48 h without a trial followed by an assessment of their memory function using the same apparatus. The vitamin E-supplementation to aged rats resulted in marked retention of their maximum memory function, although normal aged rats showed a significant memory loss of about 60%. Pyrroloquinoline quinone (PQQ), which increases in the production of nerve growth factor, and protects neurons, had a similar effect on cognitive function to that of vitamin E in the aged rats. These results suggest that vitamin E may improve cognitive deficit caused through aging by not only its neuro-protecting effect but an antioxidant efficacy.

Effects of dietary vitamin E supplementation on antioxidant enzyme activities in Litopenaeus vannamei (Boone, 1931) exposed to acute salinity changes

This study examined the effects of dietary tocopheryl acetate (vitamin E) and salinity on muscle superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) activity and gill Na +/K +-ATPase activity in Litopenaeus vannamei. Three diets containing 0, 100 and 600 mg tocopheryl acetate kg − 1 diet, respectively, were fed to shrimp (40–50 mg) for 35 days. Subsequently, shrimp were subjected to an acute salinity change (30‰ to 5, 15, 30, and 50‰) for 24 h. Significantly ( P < 0.05) increased SOD, CAT, GPX and Na +/K +-ATPase activities were observed in shrimp fed diets supplemented with vitamin E compared to shrimp fed the unsupplemented control diet. In addition, when exposed to 5 and 50‰, total SOD, CAT and GPX activities of shrimp in all dietary groups were decreased ( P < 0.05) compared to shrimp held in 30‰, with the exception of SOD in shrimp fed E-600 at 50‰ and GPX in shrimp fed E-100 at 5‰, which did not show a significant decrease (P > 0.05). A similar trend was observed in Na +/K +-ATPase activity of shrimp fed the control diet. Na +/K +-ATPase activity of shrimp fed the vitamin E-supplemented diet showed no significant variation response to acute salinity changes. Supplementation of vitamin E in diet could enhance the resistance of shrimp to acute changes in salinity. However, the higher dose of vitamin E supplement was not significantly different from the moderate dose. The results demonstrated that vitamin E might have a potentially useful role as an effective antioxidant by regulating osmotic balance and resistance to salinity changes in shrimp.

Effect of dietary supplementation with vitamin E on characteristics of vacuum-packed lamb

The effect of dietary vitamin E supplementation on lamb during vacuum-packed storage was studied. Thirty-six weaned male Manchego breed lambs were offered four dietary treatments (20, 270, 520 and 1020 mg vitamin E kg−1 feed). Lambs were fed the vitamin E-supplemented diet from 13 until 26 kg live weight. Pieces of M. longissimus dorsi were stored under vacuum at 2 ± 1 °C in the dark and meat quality was assessed after 5, 14 and 28 days of storage. Dietary supplementation significantly increased the α-tocopherol concentration in the muscle (P < 0.001). Initially, lipid oxidation, meat colour and bacterial load were similar in all groups. In meat of non-supplemented lambs the thiobarbituric acid reactive substance value increased throughout storage, whereas in meat of supplemented lambs it did not increase. Meat pigments and discolouration proportion were significantly affected by storage time (P < 0.001). The bacterial load was low initially, but after 28 days of storage it was close to 7 log10 colony-forming units (cfu) cm−2 and Enterobacteriaceae surpassed the limit of acceptability of 2.5 log10 cfu cm−2, making the lamb unsuitable for human consumption. Meat of supplemented lambs displayed less lipid oxidation than that of their non-supplemented counterparts, while meat colour and bacterial load were not affected by supplementation. Copyright © 2007 Society of Chemical Industry

In Vivo Antioxidant Activity of Methanol Extract from Quinoa Fermented with Rhizopus oligosporus

Previously, this author reported that the fermentation of quinoa with Rhizopus oligosporeus increased antioxidant activity, and the antioxidant activity of the 80% methanol extract of the fermented quinoa (Q-tempeh) was higher than the other extracts with n-hexane and water in vitro. In this paper, to clarify a beneficial effect of the fermentation of quinoa with R. oligosporus, the antioxidant activity of 80% methanol extract of Q-tempeh was investigated in rats ex vivo and in vivo. In the ex vivo experiment, the 80% methanol extract from Q-tempeh increased both activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the liver, and accelerated the production of 12-hydroxyeicosatetraenoic acid (12-HETE) in the lung. In rats fed vitamin E-free diets with 80% methanol extract of Q-tempeh, the alpha-tocopherol concentration, thiobarbituric acid-reactive substance (TBARS) value, and activities of GSH-Px and SOD in serum showed a similar concentration to those of the control rats fed a vitamin E-supplemented diet. However, the hepatic GSH-Px and SOD activities were higher than those in the control rats. On the other hand, in rats fed a vitamin E-free diet with the 80% methanol extract of quinoa, the serum alpha-tocopherol level was lower, and both TBARS values of serum and liver were higher than those in the control rats. From these results, the 80% methanol extract of Q-tempeh was inferred to be an active superoxide scavenger and peroxide reducer in vivo.

Vitamin E Supplementation Does Not Alter Azoxymethane-Induced Colonic Aberrant Crypt Foci Formation in Young or Old Mice

Vitamin E, part of the body's primary lipid-soluble defense against free radicals and reactive oxygen molecules, has been suggested to reduce the risk for some cancers. However, the role of vitamin E in the etiology and prevention of colon cancer, especially in the highest risk group, the aged, is not clear. Thus, this study was conducted to elucidate the effect of vitamin E supplementation on susceptibility to colon cancer by examining azoxymethane (AOM)-induced aberrant crypt foci (ACF) formation, a surrogate biomarker of colon cancer. Young (3-4 mo) and old (19-20 mo) C57BL/6JNIA mice were fed either a control diet (30 mg dl-alpha-tocopheryl acetate/kg diet) or a vitamin E-supplemented diet (500 mg dl-alpha-tocopheryl acetate/kg diet) for 16 wk. After 6 wk of dietary supplementation, young and old mice were injected with saline or AOM weekly for 5 wk to receive the same total dose of AOM (2.2 mg) and killed 10 wk after the first AOM injection. Vitamin E supplementation had no effect on the number of AOM-induced ACF in young or old mice. In addition, vitamin E supplementation did not have an effect on splenocyte interferon-gamma, interluekin-6 and tumor necrosis factor-alpha levels, natural killer cell killing activity or colonic cell proliferation in young or old mice. Thus, alpha-tocopherol does not seem to affect the initiation and early promotion stages of AOM-induced colon carcinogenesis in young or old mice. Whether vitamin E supplementation might be effective in reducing AOM-induced colon tumors is unclear.

Egg production, egg quality, and lipid peroxidation status in laying hens maintained at a low ambient temperature (6°C) and fed a vitamin C and vitamin E-supplemented diet

This experiment was conducted to evaluate the effects of vitamin C (L-ascorbic acid) and vitamin E (&amp;alpha;-tocopherol acetate) on egg production, egg quality, lipid peroxidation status (measured as MDA), and some serum metabolites in laying hens (Hy-Line) maintained at a low ambient temperature (6&amp;deg;C). One hundred and twenty laying hens (18-wk-old) were divided into four groups, 30 hens per group. The laying hens were fed either a basal diet or the basal diet supplemented with either 250 mg of L-ascorbic acid/kg of diet, 250 mg of &amp;alpha;-tocopherol acetate/kg of diet or 250 mg of L-ascorbic acid plus 250 mg of &amp;alpha;-tocopherol acetate/kg of diet. Although feed consumption of the hens was similar (P &amp;gt; 0.05) among treatments, supplemental vitamin C and E significantly increased final body weight, egg production, and improved feed efficiency (P &amp;lt; 0.05). Egg weights were also greater (P &amp;lt; 0.05) in hens supplemented with the combination of vitamin C and E than that of hens supplemented either vitamin or no vitamin (control). Haugh unit did not change upon each vitamin supplementation, but the combination of the vitamin supplement yielded a higher Haugh unit (P &amp;lt; 0.05). Each dietary supplement of vitamin C and vitamin E improved the egg quality (P &amp;lt; 0.05) resulting in a greater specific gravity, thicker egg shell, and heavier egg shell weight. Separately or as a combination, supplemental vitamin C and E decreased MDA, glucose, cholesterol, and triglyceride concentrations (P &amp;lt; 0.05). Results of the present study showed that supplementing vitamin C and vitamin E, particularly as a combination, improved the performance of cold-stressed laying hens, offering a potential protective management practice in preventing cold stress-related losses in performance of laying hens. Results of the present study also indicated that the effects of vitamin C and vitamin E are additive.

Dietary supplementation with vitamin E modulates avian intestinal immunity.

The effect of dietary vitamin E on immunoglobulin A (IgA) antibody production, which acts as the first line of defence at the intestinal mucosa, has not been evaluated in chickens. In the present study the impact of the inclusion of supplementary levels of vitamin E to the diet, on total and antigen-specific IgA antibody titres, T-cell subsets and Ia+ cells, was assessed. From hatching, chickens received a maize-based diet which was supplemented with either 25, 250, 2500 or 5000 mg dl-alpha-tocopherol acetate/kg. Primary immunisation with tetanus toxoid (T. toxoid) emulsified in a vegetable oil-in-water adjuvant was administered by the intraperitoneal route at 21 d of age. At 35 d of age all birds received an oral booster vaccination of T. toxoid. Significantly higher total IgA antibody titres were present in the day 42 intestinal scrapings of birds receiving the 5000 mg/kg vitamin E-supplemented diet (VESD) (P=0.05) and a notable increase was observed in birds receiving the 250 mg/kg VESD (P=0.06). At days 21 and 42 total serum IgA antibody titres of birds receiving the 250 mg/kg VESD was significantly higher (P<0.05) than the control birds. Following immunisation with T. toxoid, birds receiving the 250 and the 5000 mg/kg VESD had elevated anti-T. toxoid IgA antibody titres in final day intestinal scrapings, which, for the latter group was statistically significant (P=0.02). Both of these groups also demonstrated increased titres of anti-T. toxoid IgA in the serum at day 42. Birds receiving the 250 mg/kg VESD exhibited a notable increase in the percentage of T-helper cells and Ia+ cells in peripheral blood on day 26. The results illustrate the potential for some levels of dietary vitamin E supplementation to act as an immunomodulator of total and antigen-specific IgA antibody.

Dietary supplementation with vitamin E modulates avian intestinal immunity

The effect of dietary vitamin E on immunoglobulin A (IgA) antibody production, which acts as the first line of defence at the intestinal mucosa, has not been evaluated in chickens. In the present study the impact of the inclusion of supplementary levels of vitamin E to the diet, on total and antigen-specific IgA antibody titres, T-cell subsets and Ia+ cells, was assessed. From hatching, chickens received a maize-based diet which was supplemented with either 25, 250, 2500 or 5000 mg dl-α-tocopherol acetate/kg. Primary immunisation with tetanus toxoid (T. toxoid) emulsified in a vegetable oil-in-water adjuvant was administered by the intraperitoneal route at 21 d of age. At 35 d of age all birds received an oral booster vaccination of T. toxoid. Significantly higher total IgA antibody titres were present in the day 42 intestinal scrapings of birds receiving the 5000 mg/kg vitamin E-supplemented diet (VESD) (P=0·05) and a notable increase was observed in birds receiving the 250 mg/kg VESD (P=0·06). At days 21 and 42 total serum IgA antibody titres of birds receiving the 250 mg/kg VESD was significantly higher (P&lt;0·05) than the control birds. Following immunisation with T. toxoid, birds receiving the 250 and the 5000 mg/kg VESD had elevated anti-T. toxoid IgA antibody titres in final day intestinal scrapings, which, for the latter group was statistically significant (P=0·02). Both of these groups also demonstrated increased titres of anti-T. toxoid IgA in the serum at day 42. Birds receiving the 250 mg/kg VESD exhibited a notable increase in the percentage of T-helper cells and Ia+ cells in peripheral blood on day 26. The results illustrate the potential for some levels of dietary vitamin E supplementation to act as an immunomodulator of total and antigen-specific IgA antibody.

Effect of Dietary Intake of Vitamin A or E on the Level of DNA Damage, Chromosomal Aberrations, and Micronuclei Induced in Freshly Isolated Rat Hepatocytes by Different Carcinogens

Hepatocytes freshly isolated from male Wistar rats fed a common diet or a vitamin A- or vitamin E-supplemented diet (each for 21, 28, or 41 days) were assayed for sensitivity to DNA breakage and cytogenetic changes induced by carcinogens. Different indirectly acting carcinogens were assayed. N-nitrosomorpholine (NMOR) was the only agent that induced DNA breaks, chromosomal aberrations, and micronuclei in all experiments. Benzo[a]pyrene (B[a]p) and dimethyldibenzo[c,g]carbazole (diMeDBC) induced only DNA breaks in all experiments. Occasionally, B[a]P induced chromosomal aberrations and micronuclei, and diMeDBC induced micronuclei, but not chromosomal aberrations. These results demonstrated that the tested carcinogens assayed at concentrations highly effective in a hypoxanthine phosphoribosyltransferase/V79 system significantly increased DNA damage, while cytogenetic changes were less frequent. In hepatocytes from rats fed vitamin A, a reduction in the severity of all three end points was observed after NMOR treatment. After B[a]P treatment, we found a reduction in DNA breaks and chromosomal aberrations; after treatment with diMeDBC, we observed a reduction in DNA breaks. Treatment with vitamin E was less effective: it reduced DNA strand breaks induced by B[a]P and partially reduced those induced by diMeDBC and NMOR and the level of micronuclei induced by NMOR and B[a]P. Both vitamins reduced the level of DNA strand breaks induced by the oxidative effect of a visible light-excited photosensitizer.

Effect of oral administration of high vitamin C and E dosages on the gilthead seabream ( Sparus aurata L.) innate immune system

The effect of the oral administration of high dosages of vitamins C and E on the innate immune system of the seabream was investigated. Gilthead seabream ( Sparus aurata L.) were fed four different diets for 45 days: a commercial diet as control, a 3 g/kg vitamin C-supplemented diet, a 1.2 g/kg vitamin E-supplemented diet or a diet containing both vitamin supplements. After 15, 30 and 45 days, serum ascorbic acid and α-tocopherol levels, growth, complement titers and head–kidney leucocyte phagocytic and respiratory burst activities were evaluated. The results showed that serum vitamin levels reflected dietary input. Fish fed the vitamin C-supplemented diet showed an enhanced respiratory burst activity, while fish fed the vitamin E-supplemented diet exhibited increased complement and phagocytic activities. All of these positive effects were found in fish fed the joint diet, as well as a synergistically enhanced respiratory burst activity at day 30. The results demonstrate that in vivo vitamins C and E exert a synergistic effect enhancing the respiratory burst activity of seabream phagocytes.