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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The generation of free oxygen radicals is believed to play an important pathogenic role in the development of various disorders. More than other tissues, the skin is exposed to numerous environmental chemical and physical agents such as ultraviolet light causing oxidative stress. In the skin this results in several short- and long-term adverse effects such as erythema, edema, skin thickening, wrinkling, and an increased incidence of skin cancer or precursor lesions. However, accelerated cutaneous aging under the influence of ultraviolet light, usually termed photoaging, is only one of the harmful effects of continual oxygen radical production in the skin. Others include cutaneous inflammation, autoimmunological processes, keratinization disturbances, and vasculitis. Vitamin E is the major naturally occurring lipid-soluble non-enzymatic antioxidant protecting skin from the adverse effects of oxidative stress including photoaging. Its chemistry and its physiological function as a major antioxidative and anti-inflammatory agent, in particular with respect to its photoprotective, antiphotoaging properties, are described by summarizing animal studies, in vivo tests on human skin and biochemical in vitro investigations. The possible therapeutic use in different cutaneous disorders, and pharmacological and toxicological aspects are discussed. Many studies document that vitamin E occupies a central position as a highly efficient antioxidant, thereby providing possibilities to decrease the frequency and severity of pathological events in the skin. For this purpose increased efforts in developing appropriate systemic and local pharmacological preparations of vitamin E are required.
J Mol Med (Berl) 1995 Jan
PMID:The role of vitamin E in normal and damaged skin. 763 44

The aim of this study was to test the effect of vitamins A and E in reducing oxyradical effects and myocardial damage after ischemia-reperfusion in the rabbit heart. Oxyradical effects were indirectly assessed by hydroperoxide initiated chemiluminescence and myocardial damage was evaluated by qualitative and quantitative electron microscopy. Left anterior coronary artery was ligated in control and vitamin-treated rabbits for 30 min and then reperfused for 10 min. Rabbits were pretreated with 150 mg vitamin E and 60,000 IU vitamin A 24 h before surgery. After 10 min of reperfusion full-thickness needle samples were obtained from five different myocardial areas (three ventricular and two septal areas) and used for the determination of hydroperoxide-initiated chemiluminescence and ultrastructural damage. In the control group, hydroperoxide-initiated chemiluminescence was 18,400 +/- 500 cpm/mg protein for the non-ischemic and non-reperfused ventricular areas, and 40,500 +/- 1,800 cpm/mg protein for ischemic-reperfused ventricular areas. In the vitamin-treated group, hydroperoxide-initiated chemiluminescence was decreased by 8% in the non ischemic and non reperfused ventricular areas and by 51-75% in the ventricular ischemic and reperfused areas. The two septal areas in the control group gave chemiluminescences of 6,800 +/- 1,200 cpm/mg protein (non ischemic-non reperfused) and 17,000 +/- 2,000 cpm/mg protein (ischemia-reperfusion). In the vitamin-treated group, chemiluminescence decreased by 4 and 58%, respectively. The ischemia-reperfused areas showed extensive edema, margination of nuclear chromatin and swollen mitochondria with disrupted cristae including rupture of the inner and outer mitochondrial membranes.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Cell Biochem 1995 Apr 12
PMID:Effect of vitamins A and E on ischemia-reperfusion damage in rabbit heart. 765 77

Substantial evidence supports the theory that free radicals, especially oxygen radicals, are involved in the process of aging. The human organisms have two ways to fight them: an enzymatic way with enzymatic intervention like superoxide dismutase, catalase... and a chemical way with the intervention of scavengers such as vitamins, cysteine, methionine, gluthatione... The aim of this work was to determine that an intakes of vitamins association: vitamin E, vitamin C and beta carotene induce an increase of singlet oxygen protection of erythrocytes' subjects. The method was based on the haemolytic effect of singlet oxygen which is generated by irradiation of hematoporphyrine at 365 nm, in 22 p. cent suspension of erythrocytes' subjects. Results show that a supply of beta carotene (15 or 30 mg/day), vitamin E (15 mg/day) and vitamin C (30 mg/day) involves an increase of singlet oxygen protection of erythrocytes of subjects. This protection appears very quickly after 15 days of treatment.
Biochem Mol Biol Int 1995 Feb
PMID:Increase of singlet oxygen protection of erythrocytes by vitamin E, vitamin C, and beta carotene intakes. 766 92

Mitochondria-rich fractions isolated from livers of rats fed diets differing in their vitamin E (E) and/or selenium (Se) contents were subjected to NADPH/ADP/Fe(3+)- dependent assays of lipid peroxidation. Addition of GSH resulted in an inhibition, or lag period, of lipid peroxidation in mitochondria from rats supplemented with E. This effect was independent of the Se status of the rats. Addition of GSH + GSSG did not potentiate the lag period over that observed with GSH alone. Significant changes in mitochondrial alpha-TH during lipid peroxidation, either in the presence or absence of GSH, were not observed. Total protein thiol (PrSH) content of native mitochondria was lower in rats fed a diet deficient in both E and Se, compared to the other dietary groups. Addition of GSH or GSH + GSSG maintained mitochondrial PrSH at higher levels during lipid peroxidation than in control assays without added GSH/GSSG. Addition of GSSG alone decreased PrSH in mitochondria prepared from all rats regardless of their E or Se status. Reduced ubiquinone-9 (U-9) and the % of total U-9 and U-10 in the reduced form were significantly decreased in liver tissue from rats fed the diet deficient in both E and Se.
Biochem Mol Biol Int 1994 Dec
PMID:Dietary vitamin E and selenium effects on resistance to oxidative stress in rat liver mitochondria. 769 94

Accumulation of oxidized low density lipoproteins in macrophages and smooth muscle cells causes foam cell formation, an initial step in atherosclerosis. Active oxygen species are considered important in the pathogenesis of the disease. Antioxidants, such as tocopherols and tocotrienols have been considered to prevent the deleterious effects of active oxygen species. We found native low density lipoproteins can stimulate directly smooth muscle cell proliferation, it is associated with an increase of protein kinase C activity. d-alpha-Tocopherol, biologically most active form of vitamin E, inhibits both cell proliferation and protein kinase C activity. The effect of d-alpha-tocopherol is not related to its radical scavenging properties. Transforming growth factor-beta secreted by smooth muscle cells as growth inhibitor. Low density lipoproteins decrease the release of transforming growth factor-beta from smooth muscle cells thus activating growth. d-alpha-Tocopherol activates the cellular release of transforming growth factor-beta. These new aspects explain the important role of low density lipoproteins and vitamin E in increasing and decreasing the risk of atherosclerosis, respectively.
Biochem Mol Biol Int 1995 Jan
PMID:New roles of low density lipoproteins and vitamin E in the pathogenesis of atherosclerosis. 773 26

Adriamycin (AD)-Fe3+ caused the inactivation of Na(+)-, K(+)-ATPase and Ca(2+)-ATPase of erythrocyte membranes during lipid peroxidation. AD-Fe3+ also induced the formation of fluorescent substances from the membranes with lipid peroxidation. The fluorescent substances were little extracted by chloroform-methanol, indicating that they were retained in the membranes. Butylated hydroxytoluene and trolox strongly inhibited both the inactivation of these ATPases and the formation of fluorescent substances with lipid peroxidation. Another antioxidant, vitamin E, slightly prevented the damage of the membranes. However, p-nitrophenyl phosphatase activity and acetylcholine esterase have lower or no susceptibility to the membrane lipid peroxidation. These results indicated that the ATPases were very sensitive to lipid peroxidation and that the membranes were modified during the peroxidation reaction.
Res Commun Mol Pathol Pharmacol 1995 Feb
PMID:Adriamycin-Fe(3+)-induced inactivation of enzymes in erythrocyte membranes during lipid peroxidation. 774 51

The authors prepared an experimental animal model of ischemia and reperfusion of the limbs to evaluate in vivo the reactive oxygen species involvement and protective role of coenzyme Q10 in reperfusion injury. A group of male rabbits (untreated group) underwent clamping of abdominal aorta for 3 hr and then declamping; at intervals blood sampling was drawn for coenzyme Q10, vitamin E, lactic acid and creatine kinase assays. Another group of male rabbits (treated group) underwent the same ischemia period but before declamping coenzyme Q10 was administered intra aorta. In untreated group, coenzyme Q10 and vitamin E plasma levels decreased while lactic acid and creatine kinase plasma levels increased during reperfusion. These data demonstrate that, after only 3 hr of ischemia, the extremities show a biochemical reperfusion injury, and this involves an increased consumption of antioxidants such as coenzyme Q10 and vitamin E. In the treated group, the increase of creatine kinase plasma levels during reperfusion was not significant, while the decrease in vitamin E was more marked.
Mol Aspects Med 1994
PMID:Protective role in vivo of coenzyme Q10 during reperfusion of ischemic limbs. 775 29

Coenzyme Q10 (CoQ10), vitamin E, triglycerides and conjugated dienes were measured in a group of 48 patients on chronic hemodialysis, in 15 uremic patients and in a control group of 10 normal subjects. CoQ10 levels were significantly lower (P < 0.001) in both hemodialytic and uremic patients compared with the normal group whereas triglycerides were significantly higher (P < 0.001) with respect to both normal subjects and uremic patients. Conjugated dienes were significantly higher (P < 0.001) in both hemodialytic and uremic patients with respect to normal subjects. The predialytic values of vitamin E were higher in hemodialytic patients with respect to both normal subjects and uremic patients whereas the postdialytic values were in the normal range. A restoration mechanism of vitamin E after hemodialytic treatment was hypothesized.
Mol Aspects Med 1994
PMID:Coenzyme Q10 levels, plasma lipids and peroxidation extent in renal failure and in hemodialytic patients. 775 33

The interaction between ubiquinones and vitamin E was studied in the inner membranes of rat liver mitochondria, liposomes and human erythrocyte plasma membranes. Free radicals were produced by addition of exogenous oxidants, and their reaction with chromanols and ubiquinone was followed by ESR and HPLC. Membranes were made deficient in ubiquinone but sufficient in alpha-tocopherol and were reconstituted with added ubiquinone. With these membrane preparations it was shown that (i) in the inner mitochondrial membranes there is a requirements for ubiquinone in the enzymatic recycling of vitamin E; (ii) succinate-ubiquinone reductase incorporated in liposomes cannot protect vitamin E in the absence of ubiquinone and (iii) in human erythrocyte plasma membranes protection against the loss of vitamin E can be provided by NADH-cytochrome-b5-dependent enzymatic recycling. We conclude that ubiquinonols (ubisemiquinones) reduce vitamin E through electron transport.
Mol Aspects Med 1994
PMID:Interactions between ubiquinones and vitamins in membranes and cells. 775 45

Plasma coenzyme Q10 (CoQ10) is currently assayed in our laboratory for its well-known diagnostic meaning; in fact plasma CoQ10 levels are inversely related to metabolic demand. Definite levels of CoQ10 are also found in white and red blood cell components, as well as in platelets. Plasma and erythrocyte CoQ10 has a well assessed antioxidant role, which was demonstrated through a series of experiments. Erythrocytes previously enriched with exogenous CoQ10 were found more resistant to a hemolysis induced by a free radical initiator. Several enzymatic activities of erythrocyte ghosts were also protected by different side chain CoQ homologues, both when reduced and, although at a lesser extent, in the oxidized state. CoQ was not effective in preventing metal-catalyzed oxidation of erythrocyte membrane enzymes, and this effect is likely to be due to lack of interaction of CoQ with the metal target. Moreover CoQ was able to protect isolated enzymes and erythrocyte membrane bound enzymes from the inactivating effect of free radicals generated by water sonolysis or radiolysis. As far as plasma lipoproteins are concerned it is well known that LDL isolated from healthy volunteers supplemented with CoQ10 are more resistant to peroxidation induced by an azoinitiator. We started to systematically investigate CoQ10 and vitamin E levels in isolated human LDL and HDL. Both CoQ10 and vitamin E concentrations, referred to protein, were found higher in LDL than in HDL. Susceptibility to exogenously applied peroxidation did not correlate with the endogeneous content of the two antioxidants, possibly on the basis of different lipid content of these lipoproteins.
Mol Aspects Med 1994
PMID:Metabolic implications of coenzyme Q10 in red blood cells and plasma lipoproteins. 775 46


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