Effects of intraperitoneally injected selenium and vitamin E in rats anesthetized with halothane.

Halothane, commonly used for anesthetizing humans and animals, is one of the most important volatile anesthetics and may cause the formation of free radicals during its biotransformation. Free radicals may lead to degeneration of liver cells. Vitamin E and glutathione peroxidase (GSH-Px) containing selenium are two natural antioxidants, and these may protect the cellular lipid and lipoproteins against oxidative damage caused by free radicals. Therefore, the purposes of the present study were to investigate the probable protective effects of intraperitoneally administered Se and vitamin E on liver enzymes and to determine some other hematological parameters in the halothane anesthesia of rats. All rats were randomly divided into five groups. The first group was used as a control, and physiological saline (0.9%) was intraperitoneally injected into these animals as a placebo. The second group was used as an anesthesia control group and was only anesthetized with halothane for two hours. The third group received intraperitoneally administered Se (Na2SeO3, 0.3 mg/200 g body weight), the fourth group vitamin E (dl-alpha-tocopheryl acetate, 100 mg/kg body weight), and the fifth group a Se plus vitamin E combination (Na2SeO3, 0.3 mg/200 g body weight + dl-alpha-tocopheryl acetate, 100 mg/kg body weight). The activities of aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase, triglycerides, erythrocyte counts, the packet-cell volume, hemoglobin concentrations and neutrophyle rates significantly increased (p < 0.05 to p < 0.01) after halothane anesthesia and returned to near control levels after Se, vitamin E and Se plus vitamin E injections. The values of cholesterol, total protein, white blood cell counts and lymphocyte rates significantly decreased (p < 0.05 to p < 0.01) in the anesthesia control group. However, the levels of albumin, total bilirubin, creatinine, the mean corpuscular volume, the mean corpuscular hemoglobin, and the mean corpuscular hemoglobin concentration were not statistically influenced. In conclusion, we have determined that halothane anesthesia affected some liver enzymes and some other biochemical and hematological parameters. Se, vitamin E and their combination may prevent the increase of liver enzymes after halothane anesthesia. Based upon these results, Se and vitamin E may play an important role in the indication of hepatic cellular injury produced by halothane.     

Effect of vitamin E on adjuvant arthritis in rats

Adjuvant arthritis was induced in rats fed a diet deficient in or supplemented with vitamin E, and its severity was scored according to the macroscopic findings of their legs, tails, and ears. The average score so obtained was higher in the vitamin E-deficient diet group than in the group of rats supplemented with vitamin E. Whereas the A/G ratio remained depressed in vitamin E-deficient rats, rats on a vitamin E-supplemented diet showed a fast recovery from A/G-ratio depression. The serum levels of beta-glucuronidase and acid phosphatase were elevated after administration of an adjuvant. The serum levels of these lysosomal enzymes showed a remarkable increase in rats fed a vitamin E-deficient diet, while the elevation in lysosomal enzyme levels in rats fed a vitamin E-supplemented diet was inhibited. The levels of thiobarbituric acid (TBA) reactants in the synovia were elevated at 2 weeks after exposure to the adjuvant and were decreased thereafter. In rats maintained on a diet supplemented with vitamin E, on the other hand, the increase in synovial level of TBA reactive substances was inhibited. These observations suggest that the aggravation of adjuvant arthritis may be associated with lipid peroxidation and that antioxidants, such as vitamin E, may be beneficial for arthritis.     

Effects of vitamin E against aluminum neurotoxicity in rats

The present study examined the protective effects of vitamin E against aluminum-induced neurotoxicity in rats. Wistar rats were given daily aluminum via their drinking water containing 1600 mg/liter aluminum chloride for six weeks. Aluminum induced a significant increase in lipid peroxidation (LPO) in hippocampus and frontal cortex. Furthermore, aluminum caused marked elevation in the levels of the glial markers (glial fibrillary acidic protein (GFAP) and S100B) and proinflammatory cytokines (TNF-alpha and IL-1beta) in both brain areas. Vitamin E treatment reduced the contents of glial markers and cytokines and the levels of LPO. In conclusion, this study demonstrates that vitamin E ameliorates glial activation and reduces release of proinflammatory cytokines induced by aluminum.     

Quercetin and vitamin E ameliorate cardio-apoptotic risks in diabetic rats

Molecular and Cellular Biochemistry - Apoptosis is upregulated in all forms of diabetes, and the mitochondria act as target in diabetes pathophysiology. Quercetin and vitamin E have both shown...     

Decreased carbon centered and hydrogen radicals in skeletal muscle of vitamin E supplemented rats.

Carbon centered and hydrogen radicals were examined using electron spin resonance techniques with 5,5 dimethyl-2-pyrroline-1-oxide in the skeletal muscle of rats fed with a control diet and a vitamin E supplemented diet containing alpha tocopherol. Carbon centered and hydrogen radical levels in the white and red muscles and the soleus of these vitamin E treated muscle fibers were decreased. These results suggest that vitamin E directly quenches these free radicals.     

Muscle reinnervation in rats treated with vitamin E]

During muscle reinnervation, a transitory phase of polyinnervation occurs. In reinnervated muscles of vitamin E deficient rats, sprouting and polyinnervation are increased with respect to reinnervated controls. In this work, polyinnervation was observed in reinnervated extensor digitorum longus (edl) muscle of rats treated with pharmacological doses of vitamin E. Sciatic nerve was crushed and edl muscle was examined electrophysiologically at 30, 40 and 60 days after denervation. The percentage of polyinnervated cells in controls peaked at 30 days and thus it decreased. In muscles of vitamin E treated rats, the time course of percentage of polyinnervated muscle cells was qualitatively the same, but it was decreased at all times.     

Peculiarities of leukotrienes metabolism in vitamin E deficiency in rats

Some changes take place in the spectrum of fatty acid, cholesterol and individual phospholipids' composition in the rat liver, under E-hypovitaminosis, that can play a considerable role in the cell damage. The level of cysteinyl leucotriene decreases in the blood and liver under E-hypovitaminosis and it rises to the control level under vitamin E correction. This demonstrates the influence of tocopherol on 5-LO pathway arachidonic acid.     

Protective effects of vitamin E against atrazine-induced genotoxicity in rats

Atrazine (2-chloro-4-(ethylamino)-6-(isopropylamino)-s-triazine) is one of the most commonly used herbicides to control grasses and weeds. The widespread contamination and persistence of atrazine residues in the environment has resulted in human exposure. Vitamin E is a primary antioxidant that plays an important role in protecting cells against toxicity by inactivating free radicals generated following pesticides exposure. The present study was undertaken to investigate the protective effect of vitamin E against atrazine-induced genotoxicity. Three different methods: gel electrophoresis, comet assay and micronucleus test were used to assess the atrazine-induced genotoxicity and to evaluate the protective effects of vitamin E. Atrazine was administered to male rats at a dose of 300 mg/kg body weight for a period of 7, 14 and 21 days. There was a significant increase (P<0.001) in tail length of comets from blood and liver cells treated with atrazine as compared to controls. Co-administration of vitamin E (100 mg/kg body weight) along with atrazine resulted in decrease in tail length of comets as compared to the group treated with atrazine alone. Micronucleus assay revealed a significant increase (P<0.001) in the frequency of micronucleated cells (MNCs) following atrazine administration. In the animals administrated vitamin E along with atrazine there was a significant decrease in percentage of micronuclei as compared to atrazine treated rats. The increase in frequency of micronuclei in liver cells and tail length of comets confirm genotoxicity induced by atrazine in blood and liver cells. In addition, the findings clearly demonstrate protective effect of vitamin E in attenuating atrazine-induced DNA damage.     

Supplementation of vitamin E and selenium prevents hyperoxaluria in experimental urolithic rats

Renal injury is considered as one of the prerequisites for calcium oxalate retention. In order to determine the role of lipid peroxidation related effects for hyperoxaluria, we evaluated the alterations in lipid peroxidation, antioxidants and oxalate synthesizing enzymes in lithogenic rats with response to vitamin E + selenium treatment. In kidney of lithogenic rats, the level of lipid peroxidation and the activities of oxalate synthesizing enzymes were found to be increased whereas the levels/activities of non-enzymatic and enzymatic antioxidants were found to be decreased. The urinary excretion of both oxalate and calcium were significantly elevated. Supplementation of lithogenic rats with vitamin E + selenium decreased the levels of lipid peroxides and the activities of oxalate synthesizing enzymes like glycolic acid oxidase (GAO), lactate dehydrogenase (LDH), xanthine oxidase (XO) with a concomitant increase in the activities of enzymatic antioxidants like superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glucose-6-phosphate dehydrogenase (G6PDH) and increased levels of non-enzymatic antioxidants like ascorbic acid, alpha-tocopherol and reduced glutathione (GSH). The urinary excretion of oxalate and calcium were normalized. The antioxidants vitamin E + selenium thereby protected from hyperoxaluria.     

Effect of oral methionine and vitamin E on blood lipid peroxidation in vitamin B6 deficient rats

Lipid peroxidation in blood of vitamin B6 deficient rats was significantly increased when compared to pair-fed controls. The observed increased lipid peroxidation in vitamin B6 deficiency was correlated with high levels of lipids, metal ions and low levels of antioxidants, alpha-tocopherol, ascorbic acid and reduced GSH. Supplementation of methionine or vitamin E along with the vitamin B6 deficient diet restored the levels of antioxidants to near normal and also protected against oxidative stress. However plasma TBARS level as well as total lipids were still elevated in M-B6 diet fed rats and normalized in E-B6-d rats.     

Effect of gamma-radiation on the content of vitamin E in rats

The dynamics of vitamin E dose-dependence in the blood serum of Vistar line male rats after the total single irradiation with 60Co gamma-quantums in 0.2; 0.5; 1.0; 3.0 and 5.0 Gy doses (during 120 days); 7.0 Gy (during 20 days); 9.0 Gy (during 15 days) were studied. The vitamin E content values both in the norm and in 0.5, 1, 2, 4, 6, 8, 10, 15, 20, 30, 45, 65, 90 and 120 days after irradiation are given. The experiment data show that the dose dependence of vitamin E products has wavelike character. The possible causes of the vitamin E level decrease under intake of small and high doses of gamma-irradiation are discussed.     

Redistribution of alimentary vitamin E in tissues of irradiated rats]

The data are presented in this paper concerning the content of lipopigments, vitamin E and malondialdehyde (MDA) in the brain and liver of rats. Excess vitamin E delivered with food was shown to be bound in tissues into complex with MDA. It is suggested that it is a labile form that reserves vitamin E. Irradiation of rats caused impairment of these complex and release of vitamin E, as well as a decrease in the lipopigment fluorescence and increase in the MDA content.