Iodine supplementation of the pregnant dam alters intestinal gene expression and immunoglobulin uptake in the newborn lamb

Excess iodine intake by the pregnant dam reduces lamb serum antibody concentration, specifically immunoglobulin G (IgG). An experiment was conducted to investigate the mechanisms under pinning the reduced serum IgG concentration at 24 h postpartum in the progeny of iodine supplemented dams. Forty-five mature twin bearing ewes (n=15/treatment) were allocated to one of three dietary treatments as follows: basal diet (Control); basal diet plus 26.6 mg of iodine per ewe per day as calcium iodate (CaIO₃); or potassium iodide (KI). Ewes were individually housed and fed from d 119 of gestation until parturition. All lambs received colostrum at 1, 10 and 18 h postpartum via stomach tube. At 1 h postpartum lambs from the control and an iodine supplemented treatment (n=10 per treatment from control and CaIO₃) were euthanised before colostrum consumption and ileal segments isolated to determine the gene expression profile of a panel of genes identified as having a role in antibody transfer. Preceding euthanasia, lambs were blood sampled for determination of serum IgG, total thyroxine and free tri-iodothyronine concentrations. Progeny of CaIO₃ supplemented dams had lower tri-iodothyronine concentrations (P<0.01) at 1 h postpartum and lower serum IgG concentrations (P<0.001) at 24 h postpartum when compared with the progeny of control dams. Iodine (CaIO₃) supplementation of the dam increased the relative expression (P<0.05) of the B2M, PIGR and MYC genes in the ileum of the lamb, before colostrum consumption; while the expression of THRB declined when compared with the progeny of C dams (P<0.01). In conclusion, the results of this study show that it is the actual inclusion of excess iodine in the diet of the ewe, regardless of the carrier element, that negatively affects passive transfer in the newborn lamb. This study presents novel data describing the relationship between maternal iodine nutrition and its effect on the thyroid hormone status and subsequent gene expression in the newborn lamb; which results in a failure of passive transfer and a decline in serum IgG concentration.     

Rumen-protected choline and vitamin E supplementation in periparturient dairy goats: effects on milk production and folate, vitamin B12 and vitamin E status

We investigated the effects of rumen-protected choline (RPC) and vitamin E (VITE) administration on milk production and status of folate, vitamin B12 and vitamin E during the periparturient period of dairy goats. Forty-eight Saanen multiparous goats were selected for the 72-day experiment, being moved to a maternity pen 30 days before expected parturition and assigned to one of the four experimental groups: control (CTR), no choline or vitamin E supplementation; choline (RPC), supplemented with 4 g/day choline chloride in rumen-protected form; vitamin E (VITE), supplemented with 200 IU/day vitamin E in rumen-protected form; and choline and vitamin E (RPCE), supplemented with 4 g/day RPC chloride and 200 IU/day vitamin E. Supplements were administered individually before the morning feed to ensure complete consumption, starting 30 days before kidding and continuing for 35 days after. During the experiment, milk yield and 4% fat-corrected milk (FCM) yield were, respectively, 210 and 350 g/day higher in RPC-supplemented goats than in non-supplemented goats. Milk fat concentration and fat yield were also increased by RPC treatment. Milk yield and composition were unaffected by vitamin E supplementation. There were no significant interactions between RPC and VITE for any of the variables measured. Plasma metabolites did not differ between treatments before and after kidding except that plasma folate at parturition was higher in RPC-supplemented goats. Neither choline nor vitamin E affected vitamin B12 plasma concentrations, while a time effect was evident after the second week of lactation, when B12 levels in each treatment group started to increase. Vitamin E administration resulted in plasma α-tocopherol levels that were 2 to 2.5 times higher than in non-supplemented goats. Overall, these results suggest that greater choline availability can improve milk production and methyl group metabolism in transition dairy goats.     

The effect of late pregnancy supplementation of ewes with vitamin E on lamb vigour

The experiment measured lamb responses to supplementation of the pregnant ewe diet with vitamin E above requirement. Crossbred ewes were mated with either Suffolk or Texel rams. Twin-bearing ewes were randomly allocated (approximately 21 months of age at allocation) to one of four treatment groups (20 ewes per group, 10 mated with Suffolk and 10 with Texel rams). Treatments imposed were 50, 100, 150 or 250 IU supplementary vitamin E per ewe per day to give a four treatment by two sire-type factorial experimental design. Ewes were fed concentrates to meet energy requirements for stage of pregnancy and hay ad libitum. Diets were introduced approximately 6 weeks before lambing. Blood samples were obtained prior to introduction of diets, 17 days after introduction of diets and within 24 h of lambing from a subset of eight ewes per treatment (32 total). Colostrum samples were obtained from 10 ewes per treatment, 12 h after birth of the first lamb. All births were observed and a lamb vigour score was assigned to each lamb 5 min after birth. At 1 and 12 h after birth, rectal temperature, and at 12 h after birth, sex, crown-rump length and BW of each lamb were recorded. Mean ewe plasma α-tocopherol concentration prior to introduction of the diets was 1.5 μg/ml (s.e.m. 0.09) and did not differ between groups. There were positive linear (P < 0.001) effects of dietary vitamin E on plasma (17 days after introduction of diets) and colostrum (12 h after birth) α-tocopherol concentrations. Lamb vigour scores were superior (P < 0.001) for lambs sired by Texel rather than Suffolk rams but there were no differences as a result of vitamin E supplementation. Lamb mortality was low and unrelated to either sire or supplementary vitamin E. Lamb birth and weaning weights were also unaffected by vitamin E supplementation. Supplementing the ewe with vitamin E therefore had no effect on any lamb measurements.     

Selenium supplement alleviated the toxic effects of excessive iodine in mice

The relationship between the iodine intake level of a population and the occurrence of thyroid diseases is U-shaped. When excessive iodine is ingested, hypothyroidism or hyperthyroidism associated with goiter might develop. The aim of the study was to evaluate the effect of Se supplementation on the depression of type 1 deiodinase (D1) and glutathione peroxidase (GSHPx) activities caused by excessive iodine. D1 activity was assayed by the method with ¹²⁵I-rT₃ as a substrate. Compared to the effect of iodine alone, iodine in combination with selenium increased the activities of D1 and GSHPx. The addition of selenium alleviated the toxic effects of iodine excess on the activities of D1 and GSHPx.     

Effects of vitamin E supplementation in the extender on frozen-thawed bovine semen preservation

The maturing sperm cells discard the majority of their cytoplasm during the final stages of spermatogenesis and lose some of their defense enzymes. The purpose of this study was to investigate the effects of vitamin E supplementation on standard semen quality parameters and antioxidant activities of frozen-thawed bovine sperm. Vitamin E was added at concentrations of 0.5, 1.0, 1.5 and 2.0 mg/ml to bovine semen cryoprotective medium. The results showed that the sperm motility and VSL, STR values in the extender supplemented with 1.0 and 1.5 mg/ml of vitamin E, were significantly higher than that of other concentrations (P < 0.05). The percentages of acrosome-intact and membrane-intact sperm were significantly improved (P < 0.05) by supplementing with 1.5 mg/ml of vitamin E. In biochemical assays, the extender supplemented with vitamin E did not exhibit significant improvement in SOD (superoxide dismutase) levels, compared with the control (P > 0.05). Compared with other groups, CAT (catalase) levels were demonstrated to be greater with the supplementation of vitamin E at 1.0 and 1.5 mg/ml (P < 0.05). The extender supplemented with 1.5 mg/ml of vitamin E caused the highest levels of glutathione peroxidase (GSH-Px), compared with other groups (P < 0.05). The glutathione (GSH) activity was significantly higher with the supplementation of 0.5, 1.0 and 1.5 mg/ml of vitamin E, compared with 2.0 mg/ml in the vitamin E group and control (P < 0.05). Moreover, increasing the doses of vitamin E decreased sperm antioxidant activities, the extender supplemented with 2.0 mg/ml of vitamin E, caused the lowest levels of GSH-Px and GSH activities, compared with other treatment groups (P < 0.05). In conclusion, the beneficial effects of vitamin E noted in this study can be attributed to the antioxidant characteristics. Vitamin E supplementation in the extender reduced the lipid peroxidation potential and improved semen quality during freezing-thawing. More researches are needed to evaluate and understand the precise physiological role of vitamin E in reproduction.     

The effects of selenium,vitamin E and their combination on the composition of fatty acids and proteins in Saccharomyces cerevisiae

The aim of our studies was to test the effect and role of vitamin E and selenium supplements on yeast cell. In this study, the effects of selenium (Se), vitamin E (Vit. E), and their combination (Se plus Vit. E) on the composition of fatty acids and proteins were examined in Saccharomyces cerevisiae strains WET136 and 522. S. cerevisiae cells were grown up in YEPD medium supplemented with Se, Vit. E or their combination. It was found that the level of stearic acid was increased in all supplemented groups (p<0·05; p<0·001). The content of saturated and unsaturated fatty acids was decreased (p<0·05; p<0·01; p<0·001) in Vit. E and Vit. E plus Se supplemented S. cerevisiae. On the other hand, Se alone caused an increase (p<0·001) in the saturated fatty acids but a decrease (p<0·05; p<0·001) in the unsaturated fatty acids. Total proteins in S. cerevisiae were significantly increased (p<0·001) by Vit. E supplement. There was no significant change observed in S. cerevisiae supplemented with Se. These findings indicate that membrane composition of S. cerevisiae is affected by both Vit. E and Se supplements. © 1997 John Wiley & Sons, Ltd.     

Effect of oral vitamin E supplementation on oxidative stress in guinea-pigs with short-term hypothermia

Effects of oral vitamin E supplementation on blood malondialdehyde (MDA), glutathione (GSH) and vitamin E levels and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) enzyme activities in acute hypothermia of guinea-pigs were investigated. Thirty male guinea pigs, weighing 500-800 g were randomly divided into one of three experimental groups: A (control, without cooling), B (hypothermic) and C (hypothermic with vitamin E supplementation). The guinea-pigs of group C received daily oral supplementation of 460 mg kg(-1) bw vitamin E for 4 days before inducing hypothermia. Twenty-four hours after the last vitamin E supplementation, the guinea-pigs of the B and C groups were cooled by immersion into cold water (10-12 degrees C), and the control guinea-pigs were immersed into water of body temperature (37 degrees C) up to the neck for 5 min without using any anaesthetic or tranquilizer. Rectal body temperatures of groups were measured and blood samples for biochemical analysis were collected immediately after the cooling. The body temperature, GSH and vitamin E levels and GSH-Px enzyme activity of hypothermic guinea-pigs were lower (p < 0.05), but SOD enzyme activity was not different (p > 0.05) from those of control animals. Although, the body temperature of hypothermic with vitamin E supplementation group was lower (p < 0.05), all other parameters of this group were not different (p > 0.05) from the controls. It was concluded that oral supplementation of vitamin E can alleviate the lipid peroxidation-induced disturbances associated with hypothermia by increasing the serum vitamin E level to normal. However, more studies are needed to prove whether this vitamin can improve quality of life during the cold seasons.     

The role of selenium in thyroid hormone metabolism and effects of selenium deficiency on thyroid hormone and iodine metabolism

Selenium deficiency impairs thyroid hormone metabolism by inhibiting the synthesis and activity of the iodothyronine deiodinases, which convert thyroxine (T₄) to the more metabolically active 3,3′-5 triiodothyronine (T₃). Hepatic type I iodothyronine deiodinase, identified in partially purified cell fractions using affinity labeling with [¹²⁵I]N-bromoacetyl reverse triiodothyronine, is also labeled with⁷⁵Se by in vivo treatment of rats with⁷⁵Se-Na₂SeO₃. Thus, the type I iodothyronine 5′-deiodinase is a selenoenzyme. In rats, concurrent selenium and iodine deficiency produces greater increases in thyroid weight and plasma thyrotrophin than iodine deficiency alone. These results indicate that a concurrent selenium deficiency could be a major determinant of the severity of iodine deficiency.     

The role of selenium in thyroid hormone metabolism and effects of selenium deficiency on thyroid hormone and iodine metabolism

Selenium deficiency impairs thyroid hormone metabolism by inhibiting the synthesis and activity of the iodothyronine deiodinases, which convert thyroxine (T₄) to the more metabolically active 3,3′–5 triiodothyronine (T₃). Hepatic type I iodothyronine deiodinase, identified in partially purified cell fractions using affinity labeling with [¹²⁵I]N-bromoacetyl reverse triiodothyronine, is also labeled with⁷⁵Se by in vivo treatment of rats with⁷⁵Se−Na₂SeO₃. Thus, the type I iodothyronine 5′-deiodinase is a selenoenzyme. In rats, concurrent selenium and iodine deficiency produces greater increases in thyroid weight and plasma thyrotrophin than iodine deficiency alone. These results indicate that a concurrent selenium deficiency could be a major determinant of the severity of iodine deficiency.     

Effect of dietary iodine on thyroid hormones and energy blood metabolites in lactating goats

Aim of this work was to evaluate if long-term dietary supplementation of potassium iodide (KI) to dairy goats can influence metabolic and hormonal parameters. Thirty Sarda crossbred dairy goats were divided into three groups, which were orally administered 0 (control group; CON), 0.45 (low iodine group; LI) or 0.90 (high iodine group; HI) mg of KI/day, respectively. The daily dose of KI (76.5% of iodine) was administered as salt dissolved in water for 8 weeks. Plasma contents of nonesterified fatty acids (NEFA), urea, glucose, insulin, free triiodothyronine (FT₃) and thyroxine (FT₄) were determined weekly. Iodine supplementation increased significantly the FT₃ hormone (P = 0.007) and FT₃/FT₄ ratio (P = 0.001) and tended to influence the FT₄ hormone (P = 0.059). An iodine level × week of sampling interaction for NEFA (P = 0.013) evidenced a temporary concentration increase in supplemented groups. The ‘Revised Quantitative Insulin Sensitivity Check Index’ increased with KI supplementation (P ⩽ 0.01). Blood urea nitrogen (BUN) and insulin were lowered (P ⩽ 0.01) by iodine supplementation (groups LI and HI; P ⩽ 0.01). The glucose concentration evidenced an iodine level × week of sampling interaction (P = 0.025) due to an unexpected and temporary increase of its concentration in the CON group. Glucose concentration was decreased by KI supplementation only in LI group (P < 0.05). In conclusion, the daily supplementation of low doses of KI can improve insulin sensitivity and decrease BUN in dairy goats.     

Effect of physical restraint on oxidative stress in mice fed a selenium and vitamin E deficient diet

Physical restraint has been associated with increased oxidative damage to lipid, protein, and DNA. The purpose of this experiment was to determine whether physical restraint would further exacerbate oxidative stress in mice fed a selenium (Se) and vitamin E (VE) deficient diet. Three-week-old mice were fed a Torula yeast diet containing adequate or deficient Se and VE. Menhaden oil was added to the deficient diet to impose an additional oxidative stress. After 4 wk feeding, half the mice in each group were restrained for 5 d in well-ventilated conical tubes for 8 h daily. Mice fed the Se and VE deficient diets had increased liver thiobarbituric acid-reactive substance (TBARS) levels and decreased liver glutathione peroxidase (GPX1) activity and α-tocopherol levels. Plasma corticosterone levels were elevated in restrained mice fed the deficient diet compared to unrestrained mice fed the adequate diet. Restraint had no effect on liver TBARS or α-tocopherol levels. Liver GPX1 activity, however, was lower in restrained mice fed the adequate diet. In addition, liver superoxide dismutase (SOD) activity was lower in the restrained mice fed the adequate or deficient diet. Thus, under our conditions, Se and VE deficient diet, but not restraint, increased lipid peroxidation in mice. Restraint, however, decreased antioxidant protection in mice due to decreased activities of GPX1 and SOD enzymes.     

The effects of erdosteine, N-acetylcysteine, and vitamin E on nicotine-induced apoptosis of hippocampal neural cells

This study investigated the frequency of apoptosis in rat hippocampal neural cells after intraperitoneal nicotine injection, examining the roles of the inflammatory markers myeloperoxidase (MPO) and tumor necrosis factor alpha (TNF-alpha) in nicotine-induced brain damage and the protective effects of three known antioxidant agents, N-acetylcysteine (NAC), erdosteine, and vitamin E. Female Wistar rats were divided into seven groups, each composed of nine rats: 2 negative control groups, 2 positive control groups, one erdosteine-treated group (500 mg/kg), one NAC-treated group (500 mg/kg), and one vitamin E-treated group (500 mg/kg). Nicotine was intraperitoneally injected at a dosage of 0.6 mg/kg for 21 days. Following nicotine injection, the antioxidants were administered orally; treatment was continued until the rats were killed. Apoptosis level in hippocampal neural cells was determined by using TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick endlabeling) method. Staining of cytoplasmic TNF-alpha in hippocampal neural cells and hippocampus MPO activity were evaluated by immunohistochemistry. Nicotine administration had no effect on local TNF-alpha production, or hippocampal MPO activity. The treatments with erdosteine, NAC and vitamin E significantly reduced the rate of nicotine-induced hippocampal neural cell apoptosis. This findings suggest that erdosteine and NAC can be as effective as vitamin E in protecting against nicotine-induced hippocampal neural cell apoptosis.     

Oxidative stress and serum paraoxonase activity in experimental hypothyroidism: effect of vitamin E supplementation

Thyroid hormones are associated with the oxidative and antioxidative status of the organism. Since data on the oxidative status of hypothyroidism are limited and controversial, we investigated the oxidant and antioxidant status and serum paraoxonase/arylesterase activities in propylthiouracil-induced hypothyroidism and examined the effect of vitamin E supplementation on this experimental model. Forty male Sprague Dawley rats were randomly divided into four groups (group 1, control; group 2, control + vitamin E; group 3, propylthiouracil; group 4, propylthiouracil + vitamin E). Plasma, red blood cell, liver, heart and skeletal muscle malondialdehyde levels were increased in the propylthiouracil-treated group compared with the control rats and were decreased in propylthiouracil + vitamin E group compared with the propylthiouracil-treated group. Vitamin E supplementation also significantly increased liver and kidney reduced glutathione levels in propylthiouracil treated animals. Serum paraoxonase and arylesterase activities were decreased in propylthiouracil treated group and vitamin E supplementation caused significant increase in serum paraoxonase activity compared with the propylthiouracil-treated rats. These findings suggest that hypothyroidism is accompanied with increased oxidative stress and vitamin E supplementation exerts beneficial effects on this situation.     

Effect of selenium and vitamin E supplementation on lipid abnormalities in plasma, aorta, and adipose tissue of Zucker rats

Twenty-nine obese female Zucker rats (fa / fa) were fed with a laboratory chow supplemented or not with a selenium-rich yeast (Selenion), or Selenion + vitamin E, or vitamin E alone. Twelve lean female Zucker rats (Fa / Fa) of the same littermates fed with the same diet were used as control. After 32 wk of diet, obesity induced a large increase in plasma insulin and lipid levels. A significant decrease in the plasma vitamin E/triglycerides ratio (p < 0.005) and an increase in plasma thiobarbituric reactive substances (TBARS) (p < 0.005) were also observed. Plasma selenium and vitamin E increased in all supplemented rats. The plasma insulin level was decreased by selenion supplementation and the vitamin E/triglycerides ratio was completely corrected by double supplementation with Selenion + vitamin E. TBARS were also efficiently decreased in two obese groups receiving vitamin E. In plasma, adipose tissue and aorta, obesity induced an increase in palmitic acid (C16:0), a very large increase in monounsaturated fatty acids (palmitoleic acid C16:l, stearic acid C18:l) associated with a decrease in polyunsaturated n-6 fatty acids (linoleic acid C18:2 n - 6, arachidonic C20:4 n - 6). These alterations in fatty acid distribution were only partly modulated by Se and vitamin E supplements. However, in the aorta, antioxidant treatment in obese rats significantly reduced the increase in C16:0 and C16:l (p < 0.05 andp < 0.01, respectively) and the decrease in arachidonic acid (p < 0.05). These changes could be beneficial in the reduction of insulin resistance and help to protect the vascular endothelium.     

In vivo effect of vitamin E on serum and tissue glycoprotein levels in perchloroethylene induced cytotoxicity

The antioxidant efficacy of vitamin E on Perchloroethylene (PER) induced cytotoxicity has been studied in rats. Feeding PER to rats for 42 days using sesame oil as vehicle alters total protein and protein bound carbohydrate components in liver and kidney of experimental animals. Supplementation of vitamin E prevented the changes observed in total protein and protein bound carbohydrate components of PER administered rats. Histopathological studies also show the effectiveness of vitamin E on PER administered rats in protecting the cellular architecture of liver and kidney from PER induced cytotoxicity.     

Combined supplementation of folic acid and vitamin E diminishes diabetes-induced embryotoxicity in rats

BACKGROUND: Oxidative stress and enhanced apoptosis may be involved in the induction of embryonic dysmorphogenesis in diabetic pregnancy. Administration of folic acid or vitamin E diminishes embryonic dysmorphogenesis. We aimed to evaluate the effect of combined treatment with folic acid and vitamin E on the disturbed development in embryos of diabetic rats. METHODS: Pregnant nondiabetic and diabetic rats were treated with daily injections of 15 mg/kg folic acid or with 5% vitamin E in the diet. A third group received combined treatment. Day 10 and day 11 embryos were evaluated for development and apoptotic profile. RESULTS: We found increased malformations, resorptions, and profound growth retardation in embryos of diabetic rats compared to control embryos. Vitamin E or folic acid alone, or the 2 compounds combined, normalized embryonic demise. Maternal diabetes caused decreased nuclear factor-kappaB (NF-kappaB) activity and B-cell lymphoma 2 (Bcl-2) protein level, and increased Bcl-2-associated x proteins (Bax) in embryos. Supplementation of vitamin E alone normalized the Bax protein level in a diabetic environment. Administration of folic acid to diabetic rats increased NF-kappaB activity and Bcl-2 protein level. Combined treatment normalized Bcl-2 and Bax protein level in a diabetic environment. CONCLUSIONS: Combined supplementation of folic acid and vitamin E to pregnant diabetic rats diminished diabetes-induced malformations and resorptions, concomitant with normalization of apoptotic protein levels. No treatment completely abolished the embryonic demise; therefore, other mechanisms than oxidative stress and apoptosis are likely to be involved in diabetic embryopathy.     

Effect of selenium supplementation on thyroid hormone levels and selenoenzyme activities in growing lambs

The aim of the present study was to evaluate the effects of selenium supplementation on thyroid hormone metabolism and selenoenzyme activities in lambs. Twelve 20-d-old male lambs were assigned to one of two diets: A (0.11 ppm Se) and B (supplemented with 0.2 ppm selenium as sodium selenite). Blood samples were collected weekly for the determination of T₃, T₄, and selenium levels. The response to thyrotropin-releasing hormone (TRH) challenge was estimated at the 11th and 20th wk. Animals were slaughtered at wk 20 and tissues were collected for enzyme determination. Plasma selenium concentration was significantly higher in supplemented lambs (p<0.001). Plasma T₃ and T₄ levels remained similar in both groups. Type I deiodinase activity (ID-I) was decreased in the liver (p<0.05) and increased in the pituitary (p<0.01) of supplemented animals. No ID-I activity was detected in the thyroid. Pituitary type II deiodinase activity (ID-II) remained unchanged. The response to TRH challenge did not differ between the two groups for both challenges, but in group B, the second TRH challenge (20th wk) resulted in a significantly higher T₃ response compared to the first one (11th wk) (p<0.05). In conclusion, the lack of effects of Se supplementation on thyroid hormone metabolism demonstrates that enzyme activity is homeostatically controlled and selenium is incorporated in that order to ensure the maintenance of thyroid hormone homeostasis.     

The effects of marginal maternal vitamin A status on penta‐brominated diphenyl ether mixture‐induced alterations in maternal and conceptal vitamin A and fetal development in the Sprague Dawley rat

BACKGROUND: Polybrominated diphenyl ether (PBDE) toxicity in rodents can be associated with disruptions in endocrine signaling. We previously reported that the penta‐BDE mixture, DE‐71, disrupts thyroid hormones and vitamin A metabolism in rats during lactation, and that this disruption is amplified in animals fed diets marginal in vitamin A. The ability of the DE‐71 to disrupt vitamin A metabolism during the prenatal period has not been evaluated. While penta‐BDE mixtures are not strong teratogens in pregnant animals fed standard commercial laboratory diets, we hypothesized that they could be teratogenic under conditions of marginal vitamin A status. METHODS : rats were fed diets containing 0.4 retinyl equivalents (RE, marginal) or 4.0 RE (adequate) of vitamin A per gram of diet. Pregnant animals were exposed to DE‐71 (0, 6, 18, 60, or 120 mg/kg) from gestation days (GD) 6–11.5, or on GD 6–19.5. RESULTS : DE‐71 treatment resulted in dose‐responsive reductions in maternal thyroid hormone and markers of vitamin A metabolism, with the latter reduction amplified in marginal vitamin A dams. Fetuses from marginal vitamin A, DE‐71‐exposed dams exhibited a dose‐responsive increase in liver retinol binding protein levels. DE‐71 treatment did not result in gross malformations; however, consistent with our hypothesis, GD 20 fetal weights were lower, and skeletal ossification was less when DE‐71 exposure occurred concomitant with a marginal vitamin A status. For several endpoints, observable effects were evident at the lowest dose tested, consistent with a dose‐response trend. CONCLUSIONS : The results of this study support the concept that marginal vitamin A status enhances the disruptive effects of DE‐71 during prenatal development. Birth Defects Research (Part B) 86:48‐57, 2009. © 2009 Wiley‐Liss, Inc.     

Influence of vitamin E on the levels of fatty acids and MDA in some tissues of diabetic rats

This study was performed to determine whether vitamin E supplementation in streptozotocin-induced diabetic rats treated with insulin could affect the levels of fatty acid composition and malondialdehyde (MDA) of brain, liver and muscle tissues. Thirty Wistar albino rats were used during the experiments. They were randomly divided into three groups, each consisting of six individuals. The first group was diabetic, the second was control, and the third was diabetic but fed vitamin E. The level of stearic acid in brain tissues decreased (p<0.05) in the second and the third groups as compared to the first group. The percentage of arachidonic and polyunsaturated fatty acids slightly decreased (p<0.05) in the diabetic group in comparison to the second and third groups. The proportion of docosahexaenoic acid significantly increased (p<0.01) in the second and third groups in contrast to the first group. The level of docosatrienoic was slightly higher (p<0.05) in the third group than in other groups. In the liver tissues, the proportion of stearic, oleic and total monounsaturated fatty acids was slightly higher (p<0.05) in the first group than in the other groups. The level of arachidonic, docosahexaenoic, unsaturated and total polyunsaturated fatty acid slightly increased (p<0.05) in the second and third groups as compared to the first group. The level of myristic and stearic acids in muscle tissue slightly increased (p<0.05) in the first group as compared to the second and third groups. The proportion of arachidonic, docosahexaenoic and unsaturated fatty acids slightly increased (p<0.05) in the second and third groups relative to the first group. The amount of MDA was slightly higher in the diabetic group than in the other groups in all tissues. The results indicate that vitamin E supplementation, in experimental diabetes could play a role in controlling the oxidative status and altered fatty acid metabolism in tissues, thereby maintaining favourable fatty acid distribution in the tissues affected by diabetic complications.