Activation of endogenous lipid peroxidation in the brain during oxidative stress induced by iron and its prevention by vitamin E

Institute of Physiology, Bulgarian Academy of Sciences, Sofia 1113, Bulgaria. (Presented by Academician of the Academy of Medical Sciences of the USSR S. E. Severin.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 109, No. 1, pp. 35–37, January, 1990.     

Effect of various doses of palm vitamin E and tocopherol on aspirin-induced gastric lesions in rats

This study examined the effects of vitamin E on the prevention of aspirin-induced gastric lesions. The study was divided into two phases. Phase 1 determined the effects of various doses of palm vitamin E on the factors affecting mucosal integrity. Thirty-two male rats of the Sprague-Dawley strain (200-250 g) were randomly divided into four groups. Group I was fed a normal diet (control), Groups II, III and IV were fed a diet supplemented with palm vitamin E in a dose of 60 mg/kg food, 100 mg/kg food and 150 mg/kg food, respectively. The rats were killed after 4 weeks of feeding for the determination of gastric malondialdehyde (MDA), acid and mucus content. There was a significant decrease in gastric MDA and gastric acid in all the palm vitamin E supplemented groups compared to control. However, these doses of palm vitamin E had no significant effect on gastric mucus. The phase 2 study determined the effect of multiple doses of palm vitamin E and tocopherol on the prevention of aspirin-induced gastric lesions. Fifty rats of the same weight and strain were randomized into seven groups. Group I was fed a normal diet; groups II to IV were fed with a palm vitamin E enriched diet in doses of 60 mg, 100 mg and 150 mg/kg food, respectively; groups V to VII were fed with a tocopherol-enriched diet in doses of 20 mg, 30 mg and 50 mg/kg food, respectively. After 4 weeks of feeding with the respective diets the rats were challenged with a single intra-gastric dose of 400 mg/kg body weight aspirin suspended in propylene glycol. The rats were killed 6 h post-aspirin exposure for the determination of gastric lesion index and gastric parameters as mentioned in the phase I study. The gastric lesions index was significantly lower in all the vitamin E groups compared to control. The lowest ulcer index was observed in the groups that received 100 mg of palm vitamin E and 30 mg tocopherol in the diet. However, there was no significant difference in ulcer indices between palm vitamin E and tocopherol-treated groups. The lower ulcer index was only accompanied by lower gastric MDA content. We conclude that both palm vitamin E in doses of 60 mg, 100 mg and 150 mg/kg food as well as tocopherol in doses of 20 mg, 30 mg and 50 mg/kg food are equally effective in preventing aspirin-induced gastric lesions. The most probable mechanism is through their ability in limiting the lipid peroxidation that is involved in aspirin-induced gastric lesions.     

Activation of lipid peroxidation and changes in vitamin E levels in the lungs during oxidative stress

(Presented by Academician of the Academy of Medical Sciences of the USSR S. E. Severin.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 113, No. 2, pp. 132–134, February, 1992.     

Effect of combination of vitamin E and umbilical cord-derived mesenchymal stem cells on inflammation in mice with acute kidney injury

Background: The objective of this study is to investigate the effect of combination of umbilical cord-derived mesenchymal stem cell (UC-MSC) and vitamin E (VitE) on inflammation in mice with acute kidney injury (AKI).

Methods: UC-MSCs were isolated from pregnant wistar mice and cultured. A total of 90 female wistar mice were randomly divided into control group, AKI group, AKI?+?VitE group, AKI?+?UC-MSC group, and AKI?+?VitE?+?UC-MSC group (18 mice in each group) which were given no treatment, normal saline, VitE, UC-MSC, and VitE?+?UC-MSC, respectively. The renal pedicles on both sides were clipped for 50?min with micro-artery clips to induce AKI. Six mice were sacrificed at days 1, 3, and 7, while blood and kidney tissues were collected to detect levels of blood urea nitrogen (BUN) and creatinine (Scr). Kidney tissues were stained by HE staining to observe pathological changes; levels of interleukin-lβ, TNF-α, interleukin-10, and β-FGF were measured by ELISA.

Results: Compared with the control group, AKI mice showed higher levels of serum BUN and Scr, tubular swelling and necrosis suggesting that AKI model was successfully established. Mice in AKI?+?VitE group, AKI?+?UC-MSC group, and AKI?+?VitE?+?UC-MSC presented better renal function than mice of AKI group. Mice from AKI?+?VitE?+?UC-MSC group showed the best renal function with the least renal tubular injury (p?p?p?Conclusions: Combination of UC-MSC and VitE significantly inhibited inflammatory reaction in kidney through the regulation of inflammatory cytokines in the microenvironment of kidney with AKI. Combination of UC-MSC and VitE presented therapeutic effect on AKI than the single use of UC-MSC or VitE.     

The effects of palm vitamin E on stress hormone levels and gastric lesions in stress-induced rats

Introduction

This study examines the effects of palm vitamin E (PVE) or α-tocopherol (α-TF) supplementation on adrenocorticotropin hormone (ACTH), corticosterone and gastric lesions in rats exposed to water-immersion restraint stress (WIRS).

Material and methods

Sixty male Sprague-Dawley rats (200-250 g) were divided into three groups. Group I: 20 rats as a control group were given a normal diet. Group II: 20 rats received oral supplementation of PVE at 60 mg/kg body weight. Group III: 20 rats received oral supplementation of α-TF at 60 mg/kg body weight. After the treatment period of 28 days, each group was further subdivided into two groups: 10 rats not exposed to stress, and the other 10 rats subjected to WIRS for 3.5 h. Blood samples were taken to measure the ACTH and corticosterone levels. The rats were then sacrificed and the stomach excised and opened along the greater curvature and examined for lesions.

Results

Rats exposed to WIRS had lesions in their stomach mucosa. Our findings showed that dietary supplementation of PVE or α-TF was able to reduce gastric lesions significantly in comparison to the stressed controls. The WIRS increased plasma ACTH and corticosterone significantly. Palm vitamin E and α-TF treatments reduced these parameters significantly compared to the stressed controls.

Conclusions

Supplementation with either PVE or α-TF reduces the formation of gastric lesions, probably by inhibiting the elevation of ACTH and corticosterone levels induced by stress.     

The effects of vitamin E on NK cell activity and lymphocyte proliferation in treated mice by 2,3,7,8-tetrachlorodibenzo-p-dioxin

The study was conducted to investigate the effects of vitamin E on NK cell activity and lymphocyte proliferation in tr eated female mice by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In chronic TCDD trial, 45 mice were divided into 5 groups, and the levels of TCDD and vitamin E were 0 and 0, 100 and 0, 100 and 20, 100 and 100, and 100 ng/kg/d and 500 mg/kg/d, respectively. In acute TCDD trial, 24 mice were divided into three groups, and the levels of TCDD and vitamin E were 0 and 0, 30 and 0, and 30 μg/kg and 100 mg/kg, respectively. The results showed chronic TCDD-treatment caused decrease tendencies of spleen NK cell activity and lymphocyte proliferation, and vitamin E 100mg/kg alleviated the decreases tendencies caused by chronic TCDD-treatment, and the lymphocyte proliferation in the group given vitamin E 100mg/kg was significantly higher than that of the chronic TCDD-treated group. Acute TCDD-treatment suppressed the NK cell activity and lymphocyte proliferation, and vitamin E 100mg/kg significantly alleviated the decrease caused by acute TCDD-treatment. These results suggested that TCDD resulted in immunotoxicity, and the toxicity of acute TCDD-treatment was severe compared with chronic TCDD, while vitamin E alleviated the immunotoxicity from TCDD.     

Immunomodulatory effects of selenium and vitamin E on alterations in T lymphocyte subsets induced by T-2 toxin

Context: T-2 toxin, a potent mycotoxin, has serious effects on immune system.

Objective: Here, the effects of a sublethal dose of this toxin on T lymphocyte sub-population levels and the potential protective effects from treatment with selenium or vitamin E were studied.

Materials and methods: After having determined the sublethal dose of the T-2 toxin in Balb/c mice hosts, the post-injection kinetics of changes in T lymphocyte sub-population (CD3⁺, CD4⁺ and CD8⁺ cells) profiles were analyzed via flow cytometry. For these studies, the selenium and vitamin E were either provided to the mice before or concurrent with the toxin.

Results: The results show that after a sublethal dose of T-2 alone, the number of CD8⁺ T-lymphocytes was significantly decreased at 12?h and normalized at 48?h. In contrast, level of CD3⁺ and CD4⁺ T-lymphocytes were significantly increased at 24?h and returned to normal after 48?h. When selenium was injected into the mice 24?h before or concurrent with the T-2, the effects on CD8⁺ cells were mitigated. Oddly, only when the selenium was given with the toxin could the effects on the CD3⁺ and CD4⁺ cells be altered. Vitamin E, when injected 24?h before or concurrent with the T-2 toxin, was only able to impact upon the CD8⁺ lymphocyte alterations induced by the toxin.

Conclusions: Compared with vitamin E, it seems that selenium could assert an important effect against the immunotoxic effects of T-2 toxin against T lymphocytes.     

锰中毒对小鼠海马区NSCs的影响及其维生素E的干预作用

目的:探讨锰中毒小鼠海马区NSCs的影响及维生素E(VE)对其干预作用。方法:将60只成年雄性昆明小鼠按体重随机分为四组,即对照组(CG)、锰中毒组(MG)、维生素E组(VG)、锰中毒加维生素E组(MVG),每组15只。用腹腔注射氯化锰的方法制作锰中毒模型,采用灌胃法进行VE给药。通过Morris水迷宫实验观察小鼠的空间学习、记忆能力,用免疫组织化学检测各组小鼠海马CA1区、DG区细胞色素c(cyt c)及齿状回颗粒下层(SGZ)(巢蛋白,nestin)的表达。结果:(1)Morris水迷宫定位航行结果:MG组的逃避潜伏期比CG组明显延长(P0.05),MVG组的逃避潜伏期比MG组明显缩短(P0.05),MVG、VG和CG三组间未见显著性差异。(2)空间探索结果:MG组穿越平台的次数比CG组明显减少(P0.05),MVG穿越平台的次数比MG明显增多(P0.05),MVG、VG和CG三组间未见显著性差异。(3)免疫组织化学结果:MG组DG区nestin的阳性表达比CG组明显减少(P0.05),MVG组的阳性表达比MG组明显增多(P0.05),MVG、VG和CG三组间未见显著性差异。MG组CA1区、DG区cyt c的阳性表达均比CG组显著增多(P0.05),MVG组的阳性表达比MG组明显减少(P0.05),MVG、VG和CG三组之间未见显著性差异。结论:锰中毒可以损害神经干细胞(NSCs),降低学习记忆能力,而VE干预可减少锰对NSCs的损害作用,可能与VE可以降低cyt c的表达有关。     

Effects of addition of vitamin E to colostrum on serum α‐tocopherol and immunoglobulin concentrations in neonatal calves

Holstein calves (n = 45) were used to evaluate the effects of the addition of vitamin E (0, 100 or 1000 IU) to colostrum on absorption of α‐tocopherol and immunoglobulin in neonatal calves. Colostrum (2 l) was fed to calves as soon as possible after birth and 12 h later. The mean colostral α‐tocopherol concentration was 2.9 μg ml^‐1 (SE = 0.4). The cows were not given vitamin E supplements prior to parturition. Increasing supplementation of α‐tocopherol increased serum α‐tocopherol at 12, 24 and 48 h after birth. Addition of 1000 IU at the first calf feeding caused maximal serum α‐tocopherol concentrations by 12 h (2.12 μg ml^‐1); no increase in serum α‐tocopherol was observed thereafter. Serum IgG at 12 and 24 h tended to be lower when 100 IU of vitamin E were added; serum IgM was unaffected by treatment. No effects were observed on body weight gain, intake, feed efficiency or scours from birth up to 35 days of age. Under the conditions of this study, addition of vitamin E increased the absorption of α‐tocopherol, but did not affect the absorption of immunglobulins.     

Potential for amelioration of aflatoxin B1-induced immunotoxic effects in progeny of white leghorn breeder hens co-exposed to vitamin E

Abstract

This study was designed to evaluate the protective activity of Vitamin E (Vit E) on the immunotoxic effects induced by aflatoxin B₁ (AFB₁) in the progeny of breeder hens. For this purpose, 192 White Leghorn (WL) layer breeder hens were divided into 12 groups (A–L) and then fed test diets for either 1, 2 or 3 weeks. Group A was kept on basal feed (2900 Kcal/kg metabolizable energy) and served as control, while group B was offered a feed supplemented with Vit E at 100?mg/Kg. Groups C–G were offered feed containing 0.1, 0.5, 2.5, 5.0, and 10.0?mg/Kg AFB₁, respectively, whereas groups H–L were offered the same dietary levels of AFB₁ along with 100?mg/Kg Vit E supplementation. Hatching eggs were shifted to an incubator on a weekly basis to get progeny chicks. Hatched chicks in each group were maintained on basal ration and then subjected to different immunological assays. Lymphoproliferative responses (against PHA-P), antibody titers (against SRBC), oxidative damage to RBC, as well as phagocytic and nitrite production potential of the peritoneal macrophages from the chicks, were all adversely impacted by hen exposure to the higher doses of AFB₁ or by increased intake (time) by the hens at a given dose of the toxin. No consistent ameliorative effects from Vit E were noted in these studies, i.e. effects seen against lower AFB₁ doses were no longer apparent with the highest doses of AFB₁. As such, for now it can be concluded that, with this particular single dose level of Vit E, AFB₁-associated immunotoxic effects in progeny chicks can potentially be mitigated by dietary intake of Vit E by their hen dams. However, this is clearly an outcome that is driven by the level of the mycotoxin present in the feed. Future studies need to examine what impact higher Vit E doses than those employed herein might have in these ameliorative outcomes.     

Effects of vitamin E on human platelet and mononuclear cell responses in vitro

Recent epidemiological studies have provided evidence supporting the potential benefits of antioxidants in coronary prevention. We have investigated the effects of vitamin E on platelets, monocytes and endothelial cells in vitro. Pre-incubation of platelets with vitamin E inhibited subsequent thrombin- (P < 0.05, n = 5), collagen- (P < 0. 0001, n = 5) and ADP-(P < 0.05, n = 4) induced platelet aggregation measured using a microtitre plate method, or conventional aggregometry. The adhesion of thrombin-activated platelets to collagen was also inhibited by vitamin E (P < 0.05, n = 8), but not by vitamin C (P > 0.05, n = 8); nor was the adhesion of unstimulated platelets significantly affected (P > 0.05, n = 8). Pre-incubation of monocytes with vitamin E inhibited their subsequent adhesion to plastic (P < 0.05, n = 9), and was also associated with an 18% reduction in adhesion to EA.hy 926 endothelial cells (n = 8), although this failed to reach statistical significance. Pre-incubation of the endothelial cells with vitamin E also significantly reduced subsequent mononuclear cell adhesion by 56% (P < 0.05, n = 3).