Studie über die Rolle des Vitamin E als Nitritscavenger und N‐Nitrosamine Inhibitor

Lathia, Dinesh; Blum, Andrea J.

doi:10.1002/lipi.19910930707

Cited by 5 publications

(7 citation statements)

References 10 publications

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“…However, our findings contradict other data, which showed that vitamin E increased NO generation and NO synthase activity (Newaz et al 1999). Our data also agree with previously published studies (Lathia & Blum 1989; Carr & Frei 2000) showing that addition of antioxidants dramatically inhibited NO‐derived nitrosating agents such as nitrite. Therefore, it could be concluded that vitamin E has a protective effect in stress by its direct chain‐breaking effect on lipid peroxidation, hence preventing the accumulation of toxic NO metabolites.…”

Section: Discussionsupporting

confidence: 93%

The effect of vitamin E on stress‐induced changes in visual evoked potentials (VEPs) in rats exposed to different experimental stress models

Yargiçoğlu¹,

Yaraş²,

Ağar³

et al. 2003

Acta Ophthalmologica Scandinavica

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ABSTRACT.Purpose: The aim of the study was to investigate the effects of vitamin E on stress-induced changes in visual evoked potentials (VEPs) and lipid peroxidation. Methods: Eight experimental groups of 10 rats per group were formed. These consisted of the control group (C); the group treated with vitamin E (E); groups exposed to cold stress (CS), immobilization stress (IS) and both cold and immobilization stress (CIS), and groups exposed to equivalent stresses and treated with vitamin E (CSE, ISE, CISE). Vitamin E was injected intramuscularly in a dose of 30 mg/kg/day. Results: Following chronic stress (15 days), plasma corticosterone concentrations in all experimental groups were significantly increased over those in C group. Vitamin E significantly decreased corticosterone levels in all stress groups compared with their respective control groups. Brain nitrite levels were significantly more elevated in all stress groups than in the C group. Vitamin E reduced retina and brain nitrite levels in all stress and E groups compared with their respective control groups. Vitamin E decreased glutathione peroxidase (GSH-Px) activity in retina and brain tissues in the CSE group, but increased it in the ISE group compared with their respective control groups. Lipid peroxidation was increased in brain and retina tissues in all stress groups as indicated by the significant increase in thiobarbituric acid-reactive substance (TBARS) levels with respect to the C group. Vitamin E produced a significant decrease in brain and retina TBARS levels in all stress groups with respect to their corresponding control groups. The mean latencies of P 1 , N 1 , P 2 , N 2 and P 3 components were significantly prolonged in all stress groups compared with the C group. Conclusion: Vitamin E returned the VEP latencies in the stress groups to control values. Our findings clearly indicated that vitamin E has the potential to prevent VEP changes caused by stress.

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Section: Discussionsupporting

confidence: 93%

The effect of vitamin E on stress‐induced changes in visual evoked potentials (VEPs) in rats exposed to different experimental stress models

Yargiçoğlu¹,

Yaraş²,

Ağar³

et al. 2003

Acta Ophthalmologica Scandinavica

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“…Above all, excessive nitrite consumption has become a focus of scientists’ concern. To date, agents capable of eliminating nitrite have been extracted from green tea 20 , vitamin C 21 , sodium erythorbate 22 and vitamin E 23 24 . Various attempts have been made to reduce the concentration of nitrite in food.…”

Section: Discussionmentioning

confidence: 99%

Boletus edulis Nitrite Reductase Reduces Nitrite Content of Pickles and Mitigates Intoxication in Nitrite-intoxicated Mice

Zhang

Gao

Feng

et al. 2015

Sci Rep

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Pickles are popular in China and exhibits health-promoting effects. However, nitrite produced during fermentation adversely affects health due to formation of methemoglobin and conversion to carcinogenic nitrosamine. Fruiting bodies of the mushroom Boletus edulis were capable of inhibiting nitrite production during pickle fermentation. A 90-kDa nitrite reductase (NiR), demonstrating peptide sequence homology to fungal nitrite reductase, was isolated from B. edulis fruiting bodies. The optimum temperature and pH of the enzyme was 45 °C and 6.8, respectively. B. edulis NiR was capable of prolonging the lifespan of nitrite-intoxicated mice, indicating that it had the action of an antidote. The enzyme could also eliminate nitrite from blood after intragastric administration of sodium nitrite, and after packaging into capsule, this nitrite-eliminating activity could persist for at least 120 minutes thus avoiding immediate gastric degradation. B. edulis NiR represents the first nitrite reductase purified from mushrooms and may facilitate subsequent applications.

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“…This could occur by free radicals or products of lipid peroxidation that are produced at sites remote from the carcinogen activation. The anticarcinogenic properties of vitamin E may also be related to its cellular role as a nitrite scavenger and nitrosamine inhibitor (45) and/or its potentiation of the immune system (46) to reduce proliferation of cancer cells. Our data confirm previous reports (47,48) which show that hepatic vitamin A depletion occurs with ethanol use and that supplemental vitamin E reduces this loss of vitamin A during ethanol use and increases it in non-ethanol-consuming animals.…”

Section: Discussionmentioning

confidence: 99%

Vitamin E inhibition of lipid peroxidation and Ethanol‐mediated promotion of esophageal tumorigenesis

Odeleye

Eskelson

Mufti

et al. 1992

Nutrition and Cancer

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Promotion of chemically induced esophageal cancer by ethanol may include the generation of highly reactive free radicals and thus may be preventable by the antioxidant vitamin E. In the present study, female C57BL/6 mice received N-nitrosomethylbenzylamine (NMBzA, 0.2 mg/kg ig) three times a week for three weeks. After this esophageal carcinogenic treatment, mice were fed a nutritionally adequate liquid diet with 30% of the calories supplied by ethanol or an isocaloric carbohydrate with or without supplemental alpha-tocopherol (142 mg/kg diet). As a marker of in vivo lipid peroxidation, exhaled ethane was collected and measured 24 hours "before" the mice were killed after 20 weeks of dietary treatment. Hepatic malondialdehyde, lipid fluorescence, and conjugated dienes were determined as markers of products of lipid peroxidation and serum aminotransferases as indexes of liver toxicity. Hepatic liver concentrations of vitamins A and E and the size and frequency of esophageal tumors were also assessed. Ethanol consumption after NMBzA administration significantly increased (p less than 0.05) the size and frequency of esophageal tumors. These ethanol-promoted effects were accompanied by increases in indexes of in vivo and accumulated products of lipid peroxidation. Similarly treated animals that received supplemental dietary vitamin E showed significant reductions (p less than 0.05) in mean tumor size and frequency of tumors as well as a decrease in the indexes of hepatic lipid peroxidation. The results suggest that promotion of NMBzA-induced esophageal tumors by ethanol may in part result from increased lipid peroxidation and that vitamin E reduces carcinogenicity of NMBzA or ethanol promoter effects by inhibiting lipid peroxidation.

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Studie über die Rolle des Vitamin E als Nitritscavenger und N‐Nitrosamine Inhibitor

Cited by 5 publications

References 10 publications

The effect of vitamin E on stress‐induced changes in visual evoked potentials (VEPs) in rats exposed to different experimental stress models

The effect of vitamin E on stress‐induced changes in visual evoked potentials (VEPs) in rats exposed to different experimental stress models

Boletus edulis Nitrite Reductase Reduces Nitrite Content of Pickles and Mitigates Intoxication in Nitrite-intoxicated Mice

Vitamin E inhibition of lipid peroxidation and Ethanol‐mediated promotion of esophageal tumorigenesis

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