Interplay between Vitamin E,Glutathione and Dihydrolipoic Acid in Protection against Lipid Peroxidation

Free radicals can disturb the intracellular homeostasis by either modification of essential free sulfhydryl groups or by inducing lipid peroxidation. The damage provoked by oxidation of sulfhydryl groups might be reversible but the damage induced by the process of lipid peroxidation is probably not reversible. The main protective constituents of the cell are thiols and vitamin E. Thiols, especially glutathione, protect the cytosol while vitamin E protects the lipid membranes against free radicals. In the scavenging of free radicals in the lipid membrane, vitamin E becomes oxidized. However continuous recycling of vitamin E by a reductase, with the cytosolic thiol glutathione as cofactor, will keep the vitamin E levels high enough to protect against lipid peroxidation. In the recycling glutathione is oxidized. Dihydrolipoic acid cannot provide directly reducing equivalents for the recycling of vitamin E by the free radical reductase. However indirectly, via the reduction of oxidized glutathione, dihydrolipoic acid can mediate the regeneration of vitamin E. One of the secondary mechanisms that mediates free radical induced damage is the rise in intracellular free Ca²⁺-concentration caused by inactivation of the endoplasmic reticulum ca²⁺-ATPase. The Ca²⁺-ATPase can be inactivated either by sulfhydryl alkylation or by lipid peroxidation. The authors used the thiol-alkylating agent N-ethylmaleimide, cystamine and ebselen. Dithiothreitol reversed the inhibition caused by all the three agents, while dihydrolipoic acid reversed the inhibition caused by ebselen. Glutathione was not able to reverse the effects of the sulfhydryl reactive agents. The reactivation of the microsomal Ca²⁺-ATPase by dihydrolipoic acid, may – besides the reduction of oxidized glutathione – contribute to the protective effect of dihydrolipoic acid on lipid peroxidation.     

Saponin-Based Nanoemulsification Improves the Antioxidant Properties of Vitamin A and E in AML-12 Cells

Our work aimed to investigate the protective effects of saponin-based nanoemulsions of vitamin A and E against oxidative stress-induced cellular damage in AML-12 cells. Saponin nanoemulsions of vitamin A (SAN) and vitamin E (SEN) were prepared by high-pressure homogenization and characterized in terms of size, zeta potential, and polydispersity index. SEN and SAN protect AML-12 cells against oxidative stress-induced cellular damage more efficiently via scavenging reactive oxygen species (ROS), and reducing DNA damage, protein carbonylation, and lipid peroxidation. These results provide valuable information for the development of nanoemulsion-based delivery systems that would improve the antioxidant properties of vitamin A and E.     

Dietary fish oil and vitamin E enhance doxorubicin effects in P388 tumor-bearing mice

In this study, four kinds of rodent diets, CO, FO, CVe, and FVe, were sued by addition of canola oil, oil mixture (fish oil + canola oil), canola oil plus vitamin E, and oil mixture plus vitamin E, respectively, to a basic diet, AIN-93G, to investigate the influence of dietary fish oil and vitamin E on doxorubicin (DOX) treatment in P388 ascitic mice. Animal life span (LS) and heart damage were recorded in mice fed the four different diets and treated with different doses of DOX. The optimal doses of DOX for antitumor effect as manifested by increased LS were 6.0 and 9.0 mg/kg. Both fish oil and vitamin E significantly enhanced this effect. On the other hand, DOX at 12.0 mg/kg induced severe heart damage, which was also significantly aggravated by both fish oil and vitamin E, as shown by both decreased LS and increased serum creatine phosphokinase activity. Fish oil and vitamin E appeared to enhance the antitumor effect of optimal doses of DOX but to aggravate cardiotoxicity owing to DOX overdose.     

Tocotrienol Rich Fraction Reverses Age-Related Deficits in Spatial Learning and Memory in Aged Rats

Little is known about the effect of vitamin E on brain function. Therefore, in this study we evaluated the effect of tocotrienol rich fraction (TRF) on behavioral impairment and oxidative stress in aged rats. Thirty-six male Wistar rats (young: 3-months-old; aged: 21-months-old) were treated with either the control (olive oil) or TRF (200 mg/kg) for 3 months. Behavioral studies were performed using the open field test and Morris water maze (MWM) task. Blood was taken for assessment of DNA damage, plasma malondialdehyde (MDA) and vitamin E, and erythrocyte antioxidant enzyme activity. Brains were also collected to measure vitamin E levels. Results showed that aged rats exhibited reduced exploratory activity, enhanced anxiety and decreased spatial learning and memory compared with young rats. DNA damage and plasma MDA were increased, and vitamin E levels in plasma and brain were reduced in aged rats. Aged rats supplemented with TRF showed a markedly reduced level of anxiety, improved spatial learning and memory, reduced amount and severity of DNA damage, a reduced level of MDA, and increased levels of antioxidant enzyme activity and plasma/brain vitamin E compared with age-matched controls. In conclusion, TRF supplementation reverses spatial learning and memory decline and decreases oxidative stress in aged rats.     

Vitamin E bei rheumatischen Erkrankungen,immunologische und klinische Wirkungen

Effects of vitamin E on immune and inflammatory responses in rheumatic diseases. In rheumatic diseases immune and inflammatory responses result in the damage of the involved tissue. The immune response is mediated by cells of the immune system, which are activated and stimulated by vitamin E, eventually resulting in an enhanced immune reaction. The inflammatory response is associated with formation of free oxygen radicals, leading to activation of the eicosanoid cascade and the cytokine system. Liberation of arachidonic acid from membrane lipids, and its oxidative transformation to eicosanoids are inhibited by vitamin E, resulting in amelioration of the inflammatory response. Moreover, vitamin E has been shown to decrease formation of adhesion molecules, and to diminish proinflammatory signaling to the nucleus of the cell. These findings demonstrate several antiinflammatory properties of Vitamin E. Free oxygen radicals are also involved in cartilage and bone destruction in rheumatoid arthritis. Findings from animal experiments argue for an osteoprotective effect of vitamin E. Some short-term clinical studies have demonstrated an amelioration of laboratory findings and clinical symptoms in patients with rheumatic diseases during supplementation with vitamin E. Studies over prolonged periods of time are needed to evaluate the effect of vitamin E on immune and inflammatory responses, on osteodestruction and on clinical symptoms in rheumatic diseases, especially with regard to the interactions with the other antioxidants of the redox chain.     

Microsomal lipid peroxidation: Effect of vitamin E and its functional interaction with phospholipid hydroperoxide glutathione peroxidase

The role of vitamin E in the protection against iron dependent lipid peroxidation was studied in rat liver microsomes and Triton-dispersed microsomal lipid micelles. In these systems, an antioxidant effect of vitamin E at a physiological ratio to phospholipids could be observed only in the presence of phospholipid hydroperoxide glutathione peroxidase (PHGPX) and glutathione. The rationale of this cooperation is discussed on the basis of the hydroperoxyl radical scavenging capacity of vitamin E and the reduction of membrane hydroperoxides by PHGPX. The scavenging of lipid hydroperoxyl radicals by vitamin E, although inhibiting propagation of the peroxidative chain, produces lipid hydroperoxides from which ferrous iron generates alkoxyl radicals that react with vitamin E almost as fast as with fatty acids. Therefore, only if membrane hydroperoxides are continuously reduced by this specific peroxidase does the scavenging of hydroperoxyl radicals by vitamin E lead to an effective inhibition of lipid peroxidation.     

Wirkungen von Vitamin E auf die Haut bei topischer Anwendung

Topical Application of Vitamin E and its Effects on the Skin A review of the literature on recent-research results regarding the topical application of vitamin E is given. Moreover, some effects of vitamin E on the skin, which have not yet been published, and possible modes of action are described. Vitamin E plays a decisive role in the protection of the whole organism. Its high biological effectiveness is due to the following characteristics: 1st Vitamin E is a very effective, lipophilic antioxidant inhibiting lipid peroxidation. 2nd Due to the branched side chain in its natural configuration, it shows a very high affinity to the biological membranes and stabilizes them by physico-chemical interactions. A locally increased vitamin E supplementation is of great use for both cosmetic and dermatological purposes as it can be proved by many examples. Because it is well capable of penetrating through the skin, a topical application is often recommended. Here are some examples of its effects in cosmetics: Vitamin E ameliorates the micro-circulation in the skin, promotes hair growth, protects against UV light, delays the ageing of the skin and positively influences skin moisture. As far as its dermatological use is concerned, it inhibits inflammatory processes, reduces gingivitis, relieves of itching, ameliorates wound healing and scarring, supports the treatment of acne and counteracts specific mycoses. The results regarding cosmetics and dermatology still require more precise mechanical explanations. We expect particular biochemical, especially biological studies on the cells, to clarify the modes of action in this research field.     

Vitamin E-Bedarf bei Zufuhr von Polyenfettsäuren

Polyunsaturated Fatty Acids and Requirements of Vitamin E The major function of vitamin E is believed to be the protection of cellular membrane lipids against oxygen free-radical attack. In animals, high intakes of polyunsaturated fatty acids without proper antioxidant protection rapidly lead to vitamin E deficiency. Since the peroxidizability of fats increases with the amount and the degree of fatty acid unsaturation, the need for vitamin E increases respectively. Foods high in polyunsaturated fatty acids require, in addition to antioxidant protection to prevent rancidity during storage (technical protection against oxidation. The exact requirements of vitamin E needed for compensating the elevated demand caused by polyunsaturated fatty acids can only be estimated from data in the literature. There are no systematic studies in humans, and the requirements depend on the particular parameter chosen to establish vitamin E deficiency. For humans, a reference value of 0.9 mg IU vitamin E per gram linoleic acid may safely be assumed. For polyunsaturated fatty acids of higher degree of unsaturation and mixtures thereof, the minimum elevated vitamin E demand can be calculated by a formula.     

维生素E的稳定性研究

在氮气保护下,研究了不同温度下维生素E的稳定性,比较了维生素E在不同溶剂（甲醇、乙醇、正已烷和油酸甲酯）中的稳定性,并研究了Fe3＋、Ca2＋、N-等金属离子对维生素E稳定性的影响。研究表明维生素E在无水甲醇溶剂中相对更稳定;金属离子Na＋严重破坏维生素E稳定性。     

Effect of dietary vitamin E levels on fatty acid profiles and nonenzymatic lipid peroxidation in the guinea pig liver

Guinea pigs were fed for five weeks with three diets containing different levels of vitamin E: LOW (but nondeficient, 15 mg of vitamin E/kg diet), MEDIUM (150 mg/kg diet), and HIGH (1,500 mg/kg diet). Dietary vitamin E supplementation did not change oxidative stress indicators in the hydrophilic compartment but increased liver α-tocopherol in a dose-dependent way and strongly decreased sensitivity to nonenzymaticin vitro liver lipid peroxidation. This last effect was already observed in group MEDIUM, and no further decrease inin vitro lipid peroxidation occurred from group MEDIUM to group HIGH. The protective effect of vitamin E againstin vitro lipid peroxidation was observed even though an optimum dietary concentration of vitamin C for this animal model was present in the three different vitamin E diets. Both HIGH and LOW vitamin E decreased percentage fatty acid unsaturation in all phospholipid fractions from membrane origin in relation to group MEDIUM. The results, together with previous information, show that both vitamin E and vitamin C at intermediate concentrations are needed for optimal protection against lipid peroxidation and loss of fatty acid unsaturation even in normal nonstressful conditions. These protective concentrations are higher than those needed to avoid deficiency syndromes.     

Effects of Dietary Vitamin E on Fertility Functions in Poultry Species

Vitamin E is found in high quantities in vegetable oils. Although vitamin E has multiple functions in humans and animals, its key function is protecting cells from oxidative damage. Since its discovery, several studies have demonstrated that vitamin E deficiency causes impaired fertility in humans and lab animals. However, the effects of vitamin E deficiency or of its supplementation on the fertility of farm animals, particularly on poultry, are less well studied. Therefore, a comprehensive review of the effects of dietary vitamin E on the fertility of poultry species is needed in order to understand the beneficial role of vitamin E in the maintenance of sperm and egg qualities. Based on the observations reviewed here, we found that a moderate amount of vitamin E in poultry diet significantly protects semen/sperm qualities in male birds and egg qualities in female birds via decreasing the lipid peroxidation in semen/sperms and eggs. This review provides an overall understanding of the effects of dietary vitamin E on fertility functions in poultry species.     

Involvement of vitamin E and protein thiols in the inhibition of microsomal lipid peroxidation by glutathione

Iron-ascorbate stimulated lipid peroxidation in rat liver microsomes can be inhibited by glutathione (GSH). The role of protein thiols and vitamin E in this process was studied in liver microsomes isolated from rats fed diets either sufficient or deficient in vitamin E and incubated at 37°C unde 100% O₂. Lipid peroxidation was induced by adding 400 μM adenosine 5′-triphosphate, 2.5 to 20 μM FeCl₃, and 450 μM ascorbic acid. One mL of the incubation mixture was removed at defined intervals for the measurement of thiobarbituric acid reactive substances (TBARS), protein thiols and vitamin E. In vitamin E sufficient microsomes, the addition of GSH enhanced the lag time prior to the onset of maximal TBARS accumulation and inhibited the loss of vitamin E. Treatment of these microsomes with the protein thiol oxidant diamide resulted in a 56% loss of protein thiols, but did not significantly change vitamin E levels. However, diamide treatment abolished the GSH-mediated protection against TBARS formation and loss of vitamin E during ascorbate-induced peroxidation. Liver microsomes isolated from rats fed a vitamin E deficient diet contained 40-fold less vitamin E and generated levels of TBARS similar to vitamin E sufficient microsomes at a 4-fold lower concentration of iron. GSH did not affect the lag time prior to the onset of maximal TBARS formation in vitamin E deficient microsomes although total TBARS accumulation was inhibited. Similar to what was previously found in vitamin E sufficient microsomes [Palamanda and Kehrer, (1992)Arch. Biochem. Biophys. 293, 103–109], GSH prevented the loss of protein thiols in vitamin E deficient microsomes. However, GSH did not protect efficiently against the loss of residual vitamin E in deficient microsomes. These data provide support for the concept that GSH protects against microsomal lipid peroxidation by maintaining protein thiols, and consequently vitamin E, in the reduced state. The lack of protection in vitamin E deficient microsomes may be related to the inability of such low levels of vitamin E to inhibit peroxidation.     

发质损伤的基础研究对发用类产品发展趋势的影响

城市环境的污染、紫外线辐射、烫发剂、漂白剂以及头发的整理(洗发、吹风和梳理)等均会造成头发不同程度的损伤。头发损伤的基础研究就是研究不同物理和化学因素对头发造成损伤的作用机理、了解头发损伤与头发结构与组分的相互关系 ,并从保护头发免受损伤的角度出发探讨发用类产品的发展趋势。     

Sources and consumption of antioxidants in the diet

Vitamin E is the most important tissue antioxidant in preventing or controlling non-specific reactions from various oxidizing species produced in normal metabolism. Through this action, the vitamin protects polyunsaturated fatty acid loss from phospholipids and consequent membrane damage. The U.S. diet has an abundance of vitamin E and normal individuals accumulate effective amounts in their tissues, which is consistent with the latest recommended dietary allowances for vitamin E as indicated by the National Research Council.     

Semisynthetic Vitamin E Derivatives as Potent Antibacterial Agents against Resistant Gram-Positive Pathogens

New 5-substituted vitamin E derivatives were semisynthesized, and their antibacterial activity against human Gram-positive and Gram-negative pathogens was evaluated. Several vitamin E analogues were active against methicillin-resistant Staphylococcus aureus (MRSA) and/or methicillin-resistant Staphylococcus epidermidis (MRSE); structure-activity relationships (SARs) are discussed. As a result, it is shown that the presence of a carboxylic acid function at the C-5 position and/or at the end of the side chain is crucial for the antibacterial activity. The bactericidal or bacteriostatic action of three compounds against MRSA and MRSE was confirmed in a time-kill kinetics study, and the cytotoxicity on human cells was evaluated. The preliminary mechanism study by confocal microscopy indicated that those vitamin E analogues led to bacterial cell death through membrane disruption.     

Protection by multiple antioxidants against lipid peroxidation in rat liver homogenate

The purpose of this study was to test the hypothesis that multiple antioxygenic nutrients provide increased protection against lipid peroxidative damage to rat liver. Rats were fed diets (i) deficient in vitamin E and selenium (Diet 1), (ii) supplemented with vitamin E and selenium (Diet 2), (iii) supplemented with (ii) and in addition trolox C,N-acetylcysteine, coenzyme Q₀, and (+)-catechin (Diet 3), or (iv) supplemented with (iii) and in addition β-carotene, ascorbic acid palmitate, canthaxanthin, and coenzyme Q₁₀ (Diet 4). Liver homogenates were obtained from three rats fed each of the diets for six weeks and were incubated at 37°C up to two hours with and without exogenous tertiary-butyl hydroperoxide (TBHP) or Cu²⁺. Lipid peroxidation was determined by measurement of thiobarbituric acid substances. Diets 2 and 3 significantly protected againstin vivo hepatic lipid peroxidation, and this protection was augmented by Diet 4. Diets 2, 3, and 4 were protective against mild oxidation induced by TBHP or Cu²⁺. During incubations with exogenous TBHP and Cu²⁺, there were only small differences between diets supplemented with antioxidants in inhibition of lipid peroxidation, indicating that diets supplemented with vitamin E and selenium (Diet 2) may have provided the maximal protection for liver. The possible mechanisms of protection provided by multiple antioxidants in diets were discussed. Protection by multiple antioxidants against lipid peroxidation may translate to prevention of peroxidative damage to human tissue, a factor in human disease.     

Antigenotoxic Effect of Chamomilla recutita (L.) Rauschert Essential Oil in Mouse Spermatogonial Cells, and Determination of Its Antioxidant Capacity in Vitro

Chamomilla recutita (L.) Rauschert (Asteraceae), popularly known as chamomile, is a plant used in traditional medicine for various therapeutic purposes. Chamomile essential oil (CEO) is particularly known to inhibit the genotoxic damage produced by mutagens in mice somatic cells. The aim of this research was to determine the inhibitory potential of CEO on the genotoxic damage produced by daunorubicin (DAU) in mice germ cells. We evaluated the effect of 5, 50, and 500 mg/kg of essential oil on the rate of sister chromatid exchange (SCE) induced in spermatogonia by 10 mg/kg of the mutagen. We found no genotoxicity of CEO, but detected an inhibition of SCE after the damage induced by DAU; from the lowest to the highest dose of CEO we found an inhibition of 47.5%, 61.9%, and 93.5%, respectively. As a possible mechanism of action, the antioxidant capacity of CEO was determined using the 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging method and ferric thiocyanate assays. In the first test we observed a moderate scavenging potential of the oil; nevertheless, the second assay showed an antioxidant capacity similar to that observed with vitamin E. In conclusion, we found that CEO is an efficient chemoprotective agent against the damage induced by DAU in the precursor cells of the germinal line of mice, and that its antioxidant capacity may induce this effect.     

Zur Problematik des Blondierens menschlicher Haare

Problems Concerning Bleaching of Human Hair The bleaching of human hair using alkaline hydrogen peroxide involves a chemical change of the coloring pigments eumelanin and pheomelanin – the bleaching proper – as well as a chemical effect on the keratinous material – i. e. hair damage. The oxidation by alkaline hydrogen peroxide may proceed by different mechanisms and via different intermediates. It is discussed whether the reactions leading to bleaching or hair damage, respectively, show preferences for particular mechanisms of hydrogen peroxide decomposition.     

Dietary fish oils and long-term malaria protection in mice

Previous studies indicate a suppressive influence of fish oils on rodent malaria. The present work was carried out to study (i) the dose-effect relation between dietary fish oils and lethality of primary malaria infection in mice; (iii) the modifying influence of vitamin E; and (iii) the effect of previous fish oil feeding on parasitemia and lethality of a rechallenge infection. For two or four weeks, groups of weanling male mice were fed a standard laboratory diet or one of eight purified diets containing various amounts of fish oil (providing 6–21% of energy). The diets were prepared with and without vitamin E. After the two-or four-week feeding period, the mice were injected intraperitoneally withPlasmodium yoelii yoelii-infected erythrocytes. Six months after the primary infection (four months after discontinuing fish oil feeding), the surviving mice were again injected intraperitoneally with parasitized red blood cells (or even better—erythrocytes, erythrocytes are used elsewhere). Primary malaria infection was lethal in mice fed standard diet alone or with fish oil and vitamin E added. In contrast, feeding a fish oil-based diet without vitamin E improved survival to at least 70% if the mice had been fed these diets for four weeks. Protection against malaria did not seem to be related to the fish oil dose used. Regardless of the previous fish oil dose, all the mice surviving the primary infection survived the rechallenge infection with low parasitaemias. The results suggest that the prooxidant nature of highly unsaturated fatty acids in fish oils may beneficially influence malaria infection, and may also increase the resistance against reinfection for some time after discontinuing fish oil intake.     

The Role of Vitamin D in Supporting Health in the COVID-19 Era

The genomic activity of vitamin D is associated with metabolic effects, and the hormone has a strong impact on several physiological functions and, therefore, on health. Among its renowned functions, vitamin D is an immunomodulator and a molecule with an anti-inflammatory effect, and, recently, it has been much studied in relation to its response against viral infections, especially against COVID-19. This review aims to take stock of the correlation studies between vitamin D deficiency and increased risks of severe COVID-19 disease and, similarly, between vitamin D deficiency and acute respiratory distress syndrome. Based on this evidence, supplementation with vitamin D has been tested in clinical trials, and the results are discussed. Finally, this study includes a biochemical analysis on the effects of vitamin D in the body’s defense mechanisms against viral infection. In particular, the antioxidant and anti-inflammatory functions are considered in relation to energy metabolism, and the potential, beneficial effect of vitamin D in COVID-19 is described, with discussion of its influence on different biochemical pathways. The proposed, broader view of vitamin D activity could support a better-integrated approach in supplementation strategies against severe COVID-19, which could be valuable in a near future of living with an infection becoming endemic.