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

The development of the atherosclerosis is mediated by the accumulation of oxidized lipids in the arterial wall. There is a relationship between average intake of dietary fat, its quality, and incidence of atherosclerosis. The goal of this work was to study the effect of different dietary fats on the coenzyme Q10 and hydroperoxide content of liver mitochondria in rabbits affected by an induced atherosclerosis. The results show that the induction of experimental atherosclerosis leads to a significant increase in hydroperoxides of rabbit liver membrane mitochondria and to a significant drop in the content of CoQ10. Furthermore, treatment of atherosclerotic rabbits with different diets resulted in an increase of membrane hydroperoxides in the group fed sunflower oil whereas the increase was significantly lower for animals fed virgin olive oil and fish oil stabilized with vitamin E (1 g/kg). CoQ10 levels only recovered partially in all groups; however, values in the sunflower oil were significantly lower as compared to corresponding values of the other groups. The use of either virgin olive oil or vitamin E stabilized fish oil in the dietary treatment of atherosclerosis appears to be a valid alternative for maintaining adequate levels of CoQ10 and hydroperoxides in liver mitochondria.
Mol Aspects Med 1997
PMID:Rabbit liver mitochondria coenzyme Q10 and hydroperoxide levels: an experimental model of atherosclerosis. 926 27

It has been widely indicated that several pathological conditions depend upon concomitant risk factors rather than a unique one and that also the putative protective factors do not act alone. For these reasons it could be useful to consider subjects that present sufficiently homogeneous lifestyles (i.e. nutrition and physical activity). We carried out an investigation in a free-living community in order to clarify the possible correlations and differences among plasma metabolic and antioxidant markers in non-agonistic athletes. When subjects were divided in two main groups according to age (35-44 and 45-54 years) without considering the activity they performed, Duncan's analysis of variance revealed that they showed similar characteristics and only triglyceride levels were different. A clear negative correlation was found between vitamin E and VO2max in both age groups, a negative correlation was also found between CoQ10 and VO2max in the younger subjects and finally CoQ10 and vitamin E were also positively correlated in this first group. It appears, therefore, that people with a higher aerobic capacity have lower circulating levels of antioxidants.
Mol Aspects Med 1997
PMID:Metabolic and antioxidant markers in the plasma of sportsmen from a Mediterranean town performing non-agonistic activity. 926 29

Six experimental groups of young (7-month-old) and aged (24-32-month-old) rats, underwent different dietary manipulations (i.e. dietary restriction and/or a vitamin E-depleted diet), and their liver mitochondria were assayed for several antioxidants and peroxidation markers. Glutathione levels were affected both by age and dietary treatment. Coenzyme Q9 and C0Q10 showed the highest levels in the oldest rats where ageing, as well as other oxidative stresses, could induce ubiquinone biosynthesis.
Mol Aspects Med 1997
PMID:Dietary restriction affects antioxidant levels in rat liver mitochondria during ageing. 926 30

Active oxygen species are reported to cause organ damage. This study was therefore designed to determine whether oxidative stress contributed to the initiation or progression of hepatic DNA damage produced by T-2 toxin. The aim of the study was also to investigate the behaviour of the antioxidants coenzyme Q10 (CoQ10), and alpha-tocopherol (vitamin E) against DNA damage in the livers of mice fed T-2 toxin. Treatment of fasted mice with a single dose of T-2 toxin (1.8 or 2.8 mg/kg body weight) by oral gavage led to 76% hepatic DNA fragmentation. T-2 toxin also decreased hepatic glutathione (GSH) levels markedly. Pretreatment with CoQ10 (6 mg/kg) together with alpha tocopherol (6 mg/kg) decreased DNA damage. The CoQ10 and vitamin E showed some protection against toxic cell death and glutathione depletion caused by T-2 toxin. Oxidative damage caused by T-2 toxin may be one of the underlying mechanisms for T-2 toxin-induced cell injury and DNA damage, which eventually lead to tumourigenesis.
Mol Aspects Med 1997
PMID:T-2 toxin-induced DNA damage in mouse livers: the effect of pretreatment with coenzyme Q10 and alpha-tocopherol. 926 32

The juvenile type of neuronal ceroid lipofuscinosis (JNCL) is a recessively inherited, progressive neurodegenerative disease. In this study the levels of the antioxidant factors coenzyme Q10 (CoQ10) and vitamin E (alpha-tocopherol) were measured in plasma samples of 29 JNCL patients and compared to 48 healthy controls. A significant reduction of the coenzyme Q10 level (0.59 +/- 0.25 microgram/ml) was observed in JNCL patients when compared to control subjects (0.80 +/- 0.26 microgram/ml). The level of vitamin E was also reduced markedly in JNCL patients when compared to controls (10.4 +/- 4.1 and 12.1 +/- 4.5 micrograms/ml, respectively). The low levels of CoQ10 and vitamin E in JNCL patients may indicate an impaired antioxidant protection in this disease.
Mol Aspects Med 1997
PMID:Evaluation of the possible role of coenzyme Q10 and vitamin E in juvenile neuronal ceroid-lipofuscinosis (JNCL). 926 33

The coenzyme Q8 (CoQ8) and alpha-tocopherol contents of different mitochondrial fractions were investigated from occipital cerebral cortices of different ages. The highest CoQ8 and vitamin E concentrations were found in non-synaptic free mitochondria (FM) fractions. In several cases heavy mitochondria (HM) fractions displayed the lowest values. Occipital cerebral cortex mitochondria contained higher CoQ9 and lower CoQ10 amounts than those typical for other brain regions.
Mol Aspects Med 1997
PMID:Coenzyme Q homologs and vitamin E in synaptic and non-synaptic occipital cerebral cortex mitochondria in the ageing rat. 926 37

Whole blood vitamin Q (ubiquinone), plasma vitamins Q and E (alpha-(alpha-)tocopherol) and free cholesterol (FC) were studied before (control or base-line value, sample I) and during open chest surgery and extracorporal circulation (samples II-IV) in 10 male IHD patients. Identity existed between control whole blood and plasma ubiquinone. During surgery an increased discrepancy with lower plasma vitamin Q levels were seen. Control plasma vitamins Q, E and FC averaged 0.88 +/- 0.16 (SE), 12.1 +/- 2.2 mg x l(-1) and 0.75 +/- 0.15 g x l(-1). Corresponding molar values were 1.02 +/- 0.17, 28.1 +/- 5.1 micromol x l(-1) and 1.94 +/- 0.74 mmol x l(-1). Vitamin Q and E decreased continuously and averaged 0.64 mg x l(-1) in sample IV (0.74 micromol x l(-1), p < 0.001) and 9.4 mg x l(-1) in sample III (21.8 micromol x l(-1), p < 0.001). Hemolysis in all sample IV vials, ruined all vitamin E determinations. When normalized for FC (NQ and NE), decreases were found to be 17 (IV) and 12% (III), respectively. Large interindividual variations existed. High control NQ and NE values allowed a larger antioxidant vitamin depletion. High NQ seemed also to be a prerequisite for NE depletion. In addition, signs indicated an active liver vitamin Q release for patients rich in control antioxidant values. It was suggested that the antioxidant vitamin depletion did not prevent from radical trauma to membrane structural lipids (especially omega-3 fatty acids or vitamin F1), less membrane fluidity, erythrocyte fragility and hemolysis.
Mol Cell Biochem 1997 Aug
PMID:Vitamins Q and E, extracorporal circulation and hemolysis. 927 52

Heart mitochondria, isolated from rats fed diets deficient or supplemented with vitamin E (E) and/or selenium (Se), were subjected to time-course assays of lipid peroxidation stimulated by ascorbate/ADP/Fe3+. Mitochondria depleted of alpha-tocopherol (alpha-TH) peroxided rapidly as assessed by formation of thiobarbituric acid reactive substances (TBARS). Formation of TBARS was strongly inhibited in mitochondria from rats fed diets supplemented with E. Selenium deficiency, reduced glutathione (GSH), glutathione disulfide (GSSG) or GSH + GSSG did not affect the course of lipid peroxidation in mitochondria from rats supplemented or deficient in E. Combined E and Se deficiency resulted in significantly lower total (oxidized+reduced) mitochondrial coenzyme Q-9 (CoQ-9) concentration compared with control rats supplemented with dietary E and Se. Time-course changes in mitochondrial alpha-TH and total CoQ-9 during oxidizing conditions were minor in +E rats. Total CoQ-9 was reduced substantially, however, during the course of lipid peroxidation in mitochondria depleted of alpha-TH. Selenium-dependent glutathione peroxidase (Se-GSHPx) activity was reduced by approximately 96% in heart cytosol, and to a somewhat lesser extent in mitochondria, by dietary Se deficiency. Non-Se GSHPx activity was not detected in heart cytosol but was detected in very small amounts in heart mitochondria. Glutathione S-transferase activity of heart cytosol was decreased in E and/or Se deficiency. The results of these experiments indicate that membrane alpha-TH was most effective in inhibiting lipid peroxidation in heart mitochondria.
Biochem Mol Biol Int 1997 Aug
PMID:Effects of vitamin E and selenium on antioxidant defense in rat heart. 928 68

The concentration and activity of cholesteryl ester transfer protein (CETP) is increased in plasma in hypercholesterolemic humans and in experimental animals fed cholesterol. While the concentration of lipo-proteins appears to be the major determinant of CETP activity, we have found previously that dietary measures and pharmacologic agents that alter their lipid composition reduce the activity of CETP in plasma (CET). Since vitamin E is lipophilic and is incorporated into lipoproteins, we have examined the question of whether it too attenuates CET in cholesterol-fed New Zealand White rabbits prior to and 14 weeks after treatment with differing doses (5, 15, 30, 45 mg/kg) of vitamin E. Plasma triglycerides (TG), cholesterol (TC) and phospholipids (Lys, Sph, Lec, PI, PE) all increased significantly to a comparable degree in the rabbits fed cholesterol compared to those fed chow (p < 0.05; p < 0.01); the levels achieved were similar in the vitamin E-treated and untreated groups. As was observed with plasma lipids, cholesteryl ester transfer (CET) was accelerated to the same degree in each of the cholesterol-fed groups independent of whether they received vitamin E compared to chow-fed controls (p < 0.01) and the distribution of cholesterol in apo-B containing lipoproteins (VLDL, IDL, and LDL) was similar in the vitamin E-treated and untreated groups. These findings indicate that vitamin E has no discernible effect on CET when cholesterol levels are markedly elevated.
Comp Biochem Physiol B Biochem Mol Biol 1997 Aug
PMID:Lack of effect of vitamin E on cholesteryl ester transfer and lipoprotein composition in cholesterol-fed rabbits. 929

Considerable interest has been raised concerning the use of natural compounds in preventing skin aging and photoaging. In the idea that the combined action of agents increasing epidermal turnover with antioxidants could be advantageous in cosmetic and therapeutic treatments, we first investigated if alpha-glycolic acid affected or prevented the antioxidant activity of vitamin E and of melatonin, two compounds found beneficial as topical photoprotectant. Assays were carried out in vitro either in a biomimetic liposomal system, or in human skin homogenates. Lipid peroxidation was monitored spectrophotometrically by the time course of lipid hydroperoxide production in liposomes and by formation of TBA reactive substances (TBARS) in skin homogenates. Glycolic acid, at 25 microM to 1 mM, showed a mild, concentration-dependent antioxidant effect in liposomes, as evaluated by a slight decrease of the peroxidation rate, while, at 1 mM, reduced TBARS production in skin homogenates by 14%. Combinations of either vitamin E or melatonin with glycolic acid, in a 1:5 to 1:200 molar ratio, resulted in a clear synergistic protection of liposomes, more evident for the combination of glycolic acid with vitamin E. An amount of synergism up to 250% and up to 80% was evaluated with vitamin E and melatonin, respectively. Consumption rate of vitamin E during peroxidation of liposomes, in the absence or in the presence of glycolic acid, suggests that regeneration of vitamin E may in part explain the observed synergism. Synergistic antioxidant activity between vitamin E and glycolic acid was also observed in skin homogenates, whereas the effect of glycolic acid on the antioxidant activity of melatonin appeared additive. However, the combination of these three compounds inhibited TBARS production almost completely. Our data provide evidence that glycolic acid can strongly potentiate the antioxidant action of melatonin and vitamin E. This may suggest the advantage of combining alpha-glycolic acid with these antioxidants in skin designed preparations, both to improve penetration and availability of antioxidants to epidermal layers and to enhance their protective potential.
Biochem Mol Biol Int 1997 Sep
PMID:Synergistic effect of glycolic acid on the antioxidant activity of alpha-tocopherol and melatonin in lipid bilayers and in human skin homogenates. 930 27


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