Comparative antioxidant effectiveness of dietary beta-carotene, vitamin E, selenium and coenzyme Q10 in rat erythrocytes and plasma

Five groups of five weanling rats were each fed a Torula yeast-based diet either unsupplemented or supplemented with 30 mg beta-carotene/kg, 30 IU vitamin E/kg, 1 mg selenium/kg or 30 mg coenzyme Q10/kg. Elevated levels of plasma aspartate aminotransferase and alanine aminotransferase are sensitive indicators of liver damage. The former enzyme was lower (P less than 0.01) in the vitamin E-, selenium- and beta-carotene-supplemented groups than in the unsupplemented control group, and the latter enzyme was lower in the vitamin E- and selenium-supplemented groups, suggesting a relatively equal effectiveness of these three antioxidants against liver damage. Erythrocytes were tested for protection against uninduced oxidative damage or that induced by 1 mmol/L bromotrichloromethane (BrCl3C) by measuring thiobarbituric acid-reactive substances (TBARS), hemoglobin, hemolysis, protein precipitation, alanine release and several enzyme activities. In untreated erythrocytes, selenium, beta-carotene and coenzyme Q10 exhibited protection by lowering (P less than 0.05) TBARS and alanine release, but only vitamin E protected against hemolysis. In BrCl3C-treated erythrocytes, vitamin E, selenium and beta-carotene protected by decreasing (P less than 0.05) protein precipitation, whereas selenium and beta-carotene decreased alanine release. The results of this study suggested that, in a manner analogous to vitamin E and selenium, beta-carotene and coenzyme Q10 function as antioxygenic nutrients.     

Dietary coenzyme Q10 and vitamin E alter the status of these compounds in rat tissues and mitochondria

Vitamin E (VE) and coenzyme Q (CQ) are essential for maintaining functions and integrity of mitochondria, and high concentrations of these compounds are found in their inner membranes. This study was conducted to examine the interaction between exogenously administered CQ10 and VE in rats. Male Sprague-Dawley rats (12 mo old) were fed a basal diet (10 IU VE or 6.7 mg RRR-alpha-tocopherol equivalent) supplemented with either 0 or 500 mg CQ10, and 0, 100 or 1310 IU VE/kg diet for 14 or 28 d. Liver, spleen, heart, kidney, skeletal muscle, brain and serum were analyzed for the levels of CQ10, CQ9 and VE. CQ10 supplementation significantly (P: < 0.05) increased CQ10 concentration in the liver and spleen (total and mitochondria) and serum, but not in other organs. Interestingly, rats supplemented with CQ10 plus 100 IU VE/kg diet had significantly higher CQ10 levels in the liver and spleen, whereas those supplemented with CQ10 plus 1310 IU VE/kg diet had lower levels, compared with those supplemented with CQ10 alone. As expected, dietary VE increased VE content in all of the organs analyzed in a dose-dependent manner. However, rats fed the basal diet supplemented with CQ10 had significantly higher VE levels in liver (total and mitochondria) than those not receiving CQ10 supplementation. CQ9 levels were higher in the liver and spleen, lower in skeletal muscle and unaltered in brain, serum, heart and kidney of rats supplemented with CQ10 compared with the controls. These data provide direct evidence for an interactive effect between exogenously administered VE and CQ10 in terms of tissue uptake and retention, and for a sparing effect of CQ10 on VE. Data also suggest that dietary VE plays a key role in determining tissue retention of exogenous CQ10.     

Effect of vitamin E,selenium and age on lipid peroxidation events in rat cerebrum

The effect of 8 and 20 weeks of dietary vitamin E (200 IU/kg diet) and/or selenium (0.2 ppm) supplementation or deficiency on oxidative processes in cerebrum of 1 and 15 month old male F344 rats was examined. After 8 weeks of treatment a 32-fold difference in plasma and a 3-fold difference in cerebrum alpha-tocopherol (a-T) level was found between vitamin E supplemented and deficient young rats. These differences were 1.8- and 1.5-fold, respectively, in old rats and increased to 8- and 2-fold differences, respectively, after an additional 12 weeks of treatment. Selenium deficiency had a significant effect on plasma glutathione peroxidase activity and a slight sparing effect on plasma a-T content. Endogenous lipid peroxides (thiobarbituric acid reactants present without incubation) in cerebrum were not correlated with a-T concentration or age. However, incubation of cerebrum homogenates with or without the addition of 0.1 mM Fe²⁺, 0.25 mM ascorbic acid, or 100 mg % acetaldehyde revealed that dietary vitamin E has a major role and selenium has a minor role in the protection against ex-vivo and possibly in vivo lipid peroxidation in cerebrum.     

Clinical and biochemical effects of coenzyme Q10, vitamin E,and selenium supplementation to psoriasis patients

ObjectiveThe aim of the present study was to evaluate clinical effects of supplementation with antioxidants to patients with severe erythrodermic (EP) and arthropathic (PsA) forms of psoriasis.MethodsFifty-eight patients were hospitalized, treated by conventional protocols, and randomly assigned to four groups. Groups EP1 and PsA1 were supplemented with coenzyme Q₁₀ (ubiquinone acetate, 50 mg/d), vitamin E (natural α-tocopherol, 50 mg/d), and selenium (aspartate salt, 48 μg/d) dissolved in soy lecithin for 30–35 d. Groups EP2 and PsA2 (placebo) received soy lecithin. Clinical conditions were assessed by severity parameters. Markers of oxidative stress included superoxide production, copper/zinc-superoxide dismutase, and catalase activities in the circulating granulocytes, in the affected epidermis, and plasma levels of nitrites/nitrates.ResultsAt baseline patients had an increased superoxide release from granulocytes (10.0 ± 0.5, 2.9 ± 0.2, and 1.5 ± 0.1 nmol/L per 10⁶ cells/h for EP, PsA, and donors, respectively), increased copper/zinc-superoxide dismutase and catalase activities in granulocytes in EP patients and decreased in PsA patients, decreased activity of copper/zinc-superoxide dismutase (0.3 ± 0.0, 1.8 ± 0.1, and 2.2 ± 0.2 U/mg protein for EP, PsA, and donors, respectively), and altered activity of catalase in psoriatic epidermis. Plasma levels of nitrites/nitrates were greater than normal in psoriatic patients. Supplementation resulted in significant improvement of clinical conditions, which corresponded to the faster versus placebo normalization of the oxidative stress markers.ConclusionSupplementation with antioxidants coenzyme Q₁₀, vitamin E, and selenium could be feasible for the management of patients with severe forms of psoriasis.     

The antioxidants vitamin E and beta-carotene protect against ethanol-induced neurotoxicity in embryonic rat hippocampal cultures.

Fetal alcohol syndrome is characterized by numerous nervous system anomalies with the developing hippocampus being highly vulnerable. Other conditions can result from maternal ethanol consumption including oxidative stress. Critical antioxidants, such as vitamin E, can be decreased and antioxidative defenses altered. Gestational day 18 rat hippocampal cultures were exposed to ethanol ranging from 400 to 2400 mg/dl (16 h). MTT assays assessed neurotoxicity. Viability was decreased dose dependently. Supplementation with vitamin E or beta-carotene afforded neuroprotection against all ethanol concentrations. Vitamin E completely ameliorated neuronal loss following 400 and 800 mg/dl ethanol. Vitamin E increased survival to 95%, 79%, 66%, and 75% during 1600, 1800, and 2000 and 2400 mg/dl ethanol compared to nonethanol treatment. Vitamin E increased viability by 38%, 23%, 12%, and 29% at 1600, 1800, 2000, and 2400 mg/dl compared to non-vitamin E-supplemented, ethanol treatment. beta-Carotene completely ameliorated cell loss from 400 mg/dl ethanol and increased survival by 18% at 1600 mg/dl and 12% at 2000 mg/dl. This study demonstrates in vitro antioxidative neuroprotection against developmental ethanol exposure and suggests that nutritional therapies incorporating antioxidants may help protect against deleterious fetal effects from maternal alcohol abuse.     

液质联用法同时测定保健食品中维生素E、维生素E乙酸酯和辅酶Q10

目的采用高效液相色谱-串联质谱法(HPLC-MS/MS),建立保健食品中维生素E、维生素E乙酸酯和辅酶Q10的检测方法。方法样品经过乙腈超声提取(50℃),采用HPLC-MS/MS法进行检测。色谱条件:采用Agilent Eclipse-plus C18(2.1 mm×50 mm,1.8μm)色谱柱,流动相为乙醇-甲醇(含0.1%甲酸)溶液,梯度洗脱,流速为0.2 ml/min,柱温为35℃。质谱条件:电喷雾离子源(ESI+),干燥气温度为250℃,鞘气流速为11 L/min,源电压为4 kV,检测方式为多重反应监测(MRM)模式。结果维生素E、维生素E乙酸酯和辅酶Q10在相应的浓度范围内与峰面积都呈良好线性关系(r>0.99),加样回收率为78.1%~96.3%,精密度RSD<6%,方法检出限在0.008μg/g^0.15μg/g。结论此方法测定快速准确、灵敏度高,专属性强,可用于保健食品中维生素E、维生素E乙酸酯和辅酶Q10的检测。     

Increase of bioavailability of coenzyme Q(10) and vitamin E

Commercial coenzyme Q(10) (CoQ(10)) and alpha-tocopherol (vitamin E) formulations often show poor intestinal absorption. Delivery of CoQ(10) and vitamin E was enhanced when used with a new formulation, NanoSolve (Lipoid GmbH, Ludwigshafen, Germany), as shown by an open, comparative monocenter, crossover study of 24 volunteers. Plasma CoQ(10) and vitamin E were determined from predose until +14 hours. To compare bioavailability, corrected maximum concentration, time to reach maximum concentration, and area under the curve from 0 to 14 hours were assessed. The NanoSolve test formulation contained 100 mg of CoQ(10) and 120 mg of vitamin E. The pure substances in hard gelatin capsules served as the reference. Although identical amounts of CoQ(10) and vitamin E were administered, absolutely higher serum concentrations of the active ingredients were achieved by the NanoSolve formulation than by the pure materials in gelatin capsules. The bioavailability of CoQ(10) increased fivefold after administration of the NanoSolve formulation, and the bioavailability of vitamin E was enhanced 10-fold both compared to the pure substances.     

Effects of oral coenzyme Q10 supplementation on sodium nitrite-induced lipid peroxidation in rats.

Studies were carried out to examine the anti-oxidative effect(s) of oral coenzyme Q10 supplementation (10 mg/kg b.w./day) in rats treated per os with either sodium nitrite (10 mg/kg b.w./day) or saline (control) for 14 days. Results showed that sodium nitrite increases thiobarbituric-acid reactive substances (TBARS in rat small intestinal mucosa and liver, and the agent did not have any effect(s) on the total anti-oxidant status (TAS) and lipid peroxidation of rat blood. Pretreatment of nitrite-poisoned rats with coenzyme Q10 mitigated TBARS and increased TAS in animal blood. Coenzyme Q10 has been found to be a promising anti-oxidant agent in sodium nitrite-induced lipid peroxidation.     

Cosupplementation with vitamin E and coenzyme Q10 reduces circulating markers of inflammation in baboons

BACKGROUND: Inflammation and oxidative stress are processes that mark early metabolic abnormalities in vascular diseases. OBJECTIVES: We explored the effects of a high-fat, high-cholesterol (HFHC) diet on vascular responses in baboons and the potential response-attenuating effects of vitamin E and coenzyme Q(10) (CoQ(10)) supplementation. DESIGN: We used a longitudinal design by subjecting 21 baboons (Papio hamadryas) to sequential dietary challenges. RESULTS: After being maintained for 3 mo on a baseline diet (low in fat and cholesterol), 21 baboons were challenged with an HFHC diet for 7 wk. The serum C-reactive protein (CRP) concentrations did not change. Subsequent supplementation of the HFHC diet with the antioxidant vitamin E (250, 500, or 1000 IU/kg diet) for 2 wk reduced serum CRP concentrations from 0.91 +/- 0.02 to 0.43 +/- 0.06 mg/dL. Additional supplementation with CoQ(10) (2 g/kg diet) further reduced serum CRP to approximately 30% of baseline (0.28 +/- 0.03 mg/dL; P = 0.036 compared with the HFHC diet). Introduction of the HFHC diet itself significantly decreased serum P-selectin (from 48.8 +/- 7.2 to 32.9 +/- 3.7 ng/dL, P = 0.02) and von Willebrand factor (from 187.0 +/- 10.1 to 161.9 +/- 9.0%, P = 0.02) concentrations. However, neither vitamin E alone nor vitamin E plus CoQ(10) significantly altered the serum concentrations of P-selectin or von Willebrand factor. CONCLUSIONS: Dietary supplementation with vitamin E alone reduces the baseline inflammatory status that is indicated by the CRP concentration in healthy adult baboons. Cosupplementation with CoQ(10), however, significantly enhances this antiinflammatory effect of vitamin E.     

Effects of coenzyme Q10 supplementation on exercise performance, VO2max, and lipid peroxidation in trained cyclists.

The effects of dietary supplementation with Coenzyme Q10 (CoQ10), a reputed performance enhancer and antioxidant, on physiological and biochemical parameters were examined. Ten male bicycle racers performed graded cycle ergometry both before and after being given 100 mg per day CoQ10 or placebo for 8 weeks. Analysis of variance showed a significant difference between groups for postsupplementation serum CoQ10. Although both groups demonstrated training related improvements in all physiological parameters over the course of the study, there were no significant differences between the two groups (p > .05). Both groups showed a 21% increase in serum MDA (an index of lipid peroxidation) after the presupplementation exercise test. After 8 weeks this increase was only 5%, and again was identical for both groups. Supplementation with CoQ10 has no measurable effect on cycling performance, VO2max, submaximal physiological parameters, or lipid peroxidation. However, chronic intense training seems to result in marked attenuation of exercise-induced lipid peroxidation.     

Endotoxin and lipid peroxidation in vitro in selenium- and vitamin E-deficient and -adequate rat tissues

The effect of Salmonella typhimurium endotoxin injected intraperitoneally into rats (0.5 mg/kg of body weight) on subsequent lipid peroxidation in vitro was assessed. Peroxidation was monitored by measuring ethane production from tissue slices, as well as thiobarbituric acid-reactive substances and conjugated dienes in tissue homogenates. Weanling rats were fed a selenium- and vitamin E-deficient basal diet or one supplemented with 0.2 mg of Se/kg of diet and 200 mg of vitamin E/kg. After 9 to 16 wk, ethane production and thiobarbituric acid-reactive substances in liver and lung generally were increased by LPS treatment of Se- and vitamin E-deficient rats. Conjugated dienes were increased by LPS treatment in liver of Se- and vitamin E-deficient rats, but paradoxically, were higher in Se- and vitamin E-adequate liver tissue. Daily injections of 1 g of hydroxyurea/kg of body weight, a cell proliferation inhibitor, for 2 d prior to LPS injection significantly decreased the LPS-induced ethane production in Se- and vitamin E-deficient rat liver and lung. These results show that low doses of LPS injected into rats stimulated lipid peroxidation in vitro in Se- and vitamin E-deficient rat liver tissue. Hydroxyurea decreased LPS-induced lipid peroxidation in vitro; this suggests that neutrophils or macrophages are involved in LPS-induced lipid peroxidation.     

Dietary vitamin E and beta-carotene sources influence vitamin A and E storage in young rats fed marginal and adequate vitamin E

The effects of two vitamin E levels (30 and 75 IU/kg diet) and the interrelation of two vitamin E sources [dl-alpha-tocopheryl acetate (dl-alpha-TA) and d-alpha-tocopheryl acid succinate (d-alpha-TAS)] and three vitamin A sources [retinyl palmitate (RP), all-trans synthetic beta-carotene (SBC), and natural beta-carotene (NBC)] were studied. Dietary vitamin A sources provided 4,000 IU/kg. Twelve groups of Fischer 344 rats (10/group) were fed designated diets for eight weeks. For RP, SBC, and NBC, the increase in each vitamin E source from a marginal to an adequate dietary level caused a significant increase in liver and heart alpha-tocopherol. Among rats fed diets with an adequate level of vitamin E, d-alpha-TAS was not as effective as dl-alpha-TA in increasing liver alpha-tocopherol levels. Plasma retinol was lower in rats fed d-alpha-TAS than in those fed dl-alpha-TA. Among rats fed diets with an adequate level of dl-alpha-TA, those fed SBC had significantly higher liver and heart alpha-tocopherol concentrations than did all other groups (p < 0.05). Liver retinol equivalents for rats fed NBC were approximately 66% lower than those in rats fed SBC or RP (p < 0.05). The roles of the two vitamin E sources in alpha-tocopherol metabolism are not equivalent. These data indicate that vitamin A source influences the magnitude of the tissue vitamin A and E changes in response to the two vitamin E sources.     

Dietary sources of vitamin A, C, E and beta-carotene in a adult Mediterranean population

OBJECTIVE: Estimation of vitamin A, C, E and beta-carotene food sources, as well as its nutritional intake and density in adult Catalonian population. METHODOLOGY: A cross-sectional study was conducted over 2,346 individuals obtained from the sample of Catalonian Survey of Nutritional Status aged 18 to 75 years old to estimate usual dietary intake of vitamins A, C, E and beta-carotene using two 24 hour dietary recalls administered in two periods (june-july and november-december of 1992). Replicated 24 hour Recalls allowed for estimation of usual intake. Calculation of food sources for vitamins encompassed three phases: foods transformation into nutrients, aggregation of foods in categories and sum of nutrients by food categories. RESULTS: Intake of vitamin A (equivalents of retinol of provitamin A and vitamin A), E, C were closely near or higher than RDA. Nutritional density of vitamin C, E and beta-carotene were higher in female group. Nutritional density was positively associated to age for vitamins C, E and beta-carotene. Addition fat was the first source of vitamin E and it reached 33.8% of total vitamin E intake. Vegetables contributed in 17.3 % to the total vitamin C, whereas fruits accounted for 57.9%. Fruits recached 40.6% of the total beta-carotene intake, whereas vegetables accounted for 34.8%. The major contributors of vitamin A were milk and dairy products. CONCLUSIONS: Nutritional intake of vitamin A, C and E are over the RDA parameters suggesting an healthy nutritional status that must be confirmed and ratify by biochemical assessment. Nutritional densities were higher in female gender than in males in vitamins C, E, and beta-carotene possibly due to a higher intake of total lipids in male gender than in females. Nutritional density was positively associated to age in the same group of vitamins, suggesting a higher intake of empty calories in younger group. Fruits and Vegetables accounted for more than 70% of vitamin C and beta-carotene and major contributors were citrics, carrots, tomatoes, spinach, and cauliflower, highlighting their importance in elaboration of dietary guide lines.     

Erythrocyte lipid peroxidation, glutathione and vitamin E levels in cholesterol-fed rats

Erythrocyte cholesterol and phospholipid levels, the susceptibility of erythrocytes to lipid peroxidation as well as erythrocyte glutathione and vitamin E levels were determined in rats fed a high cholesterol (2%, w/w) and high cholic acid (0.5%, w/w) diet for 3 months. Cholesterol feeding caused an increase in erythrocyte cholesterol levels, but no change was observed in erythrocyte phospholipid levels. Dietary cholesterol did not alter the susceptibility of erythrocytes to lipid peroxidation as well as erythrocyte glutathione and vitamin E levels in rats.     

Effect of chronic consumption of ethanol and vitamin E on fatty acid composition and lipid peroxidation in rat heart tissue.

Lipid peroxidation products and the fatty acid composition of phospholipids were studied in the hearts of rats chronically consuming ethanol supplemented with large amounts of vitamin E. Ethanol representing 36% of the total calories was ingested for 7 weeks in a modified Lieber-DeCarli liquid diet that contained vitamin E at 30 IU/L in the control or 172 IU/L in the supplemental dietary group. Ethanol and/or vitamin E did not change the absolute content (micrograms per mg of phospholipids) of the main fatty acids (C18:0, C18:2, and C20:4) of heart phospholipids but increased the amount of the minor C20-C22 fatty acids. Cardiac phospholipid levels increased in rats chronically consuming excess vitamin E and/or alcohol. Chronic ethanol consumption caused elevations of the relative content (percent of total fatty acids) of tri-, tetra-, and hexaenoic acids and peroxidizability index (PI) of the cardiac phospholipids. Supplementation with vitamin E blocked this ethanol-induced shift in the fatty acid profile toward unsaturation and decreased the PI. Ethanol enhanced accumulation of vitamin E in heart tissue by 30% irrespective of the vitamin E content in the diet. Enrichment of the diet with vitamin E coincided with the low levels of fluorescent products in heart lipids. A positive correlation (r = 0.36; p = 2%) was found between vitamin E and diene conjugates in the heart cells. Thus, vitamin E has a stabilizing effect on heart phospholipids by preventing changes in their fatty acid composition and peroxidative deterioration.     

Augmenting effect of vitrification on lipid peroxidation in mouse preantral follicle during cultivation: Modulation by coenzyme Q10

Cryopreservation-induced oxidative stress (OS) may lead to lipid peroxidation, which may be responsible for decreased cell survival rate. Coenzyme Q10 (CoQ10) as a potent antioxidant may improve cell viability by neutralizing OS. In this study, oxidative lipid injury following the vitrification of preantral follicles was investigated. The effects of CoQ10 treatment on the malondialdehyde (MDA) levels, lipid peroxidation products, and activities of enzymatic and nonenzymatic antioxidants of vitrified preantral follicles were also studied. Preantral follicles were isolated from immature mouse ovaries and were vitrified. After warming, these follicles were cultured with or without CoQ10 for four days. The levels of total antioxidant capacity (TAC) and MDA, as well as the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT), were assessed at 0, 24, 48, 72, and 96 hours of culture period. The MDA level in the vitrified preantral follicles was higher than that in the fresh groups. By contrast, the MDA level was significantly lower in the groups with CoQ10 treatment than in those without this treatment during cultivation. The TAC level was higher in the fresh preantral follicles than in the vitrified groups. The rates were also higher in the CoQ10-treated groups than in those without this treatment. The activities of SOD, GPX, and CAT were also significantly higher in the fresh groups than in the vitrified groups, especially in the groups with CoQ10 treatment than in those without this treatment. Lowering the vitrification-induced lipid peroxidation of preantral follicles by CoQ10-supplemented maturation medium may be mediated by increasing SOD, GPX, and CAT activities and TAC level during cultivation.     

Coenzyme Q(10), vitamin E, selenium, and methionine in the treatment of chronic recurrent viral mucocutaneous infections

ObjectiveHost defense and latency determinants in viral recurrent dermatologic infections are not entirely understood, as conventional protocols are inadequate to achieve fast healing and relapse prevention. Endogenously produced oxygen/nitrogen reactive species (ROS/RNS) are essential for antiviral immune defense, while their excess may aggravate skin inflammation. Here, we sought a nutritional approach capable of controlling ROS/RNS balance to accelerate recovery and inhibit recurrences of two mucocutaneous chronic DNA-virus infections.MethodsTwo controlled clinical trials evaluated the feasibility of ROS/RNS-modulating nutriceutical dosages of coenzyme Q₁₀, RRR-α-tocopherol, selenium aspartate, and L-methionine associated with established therapies. Clinical trial 1 evaluated 68 patients with relapsing human papillomavirus skin warts treated with cryotherapy followed by 180 d of nutriceutical/placebo administration. Clinical trial 2 compared the combination of acyclovir followed by 90 d of nutriceutical administration versus acyclovir alone in patients with recurrences of herpes simplex genitalis (n = 60) or herpes zoster (n = 29). Viral DNA levels were assessed by polymer chain reaction, biomarkers of antiviral defense (peroxynitrite and IFNα/γ) and antioxidant capacity (lipophilic antioxidants and glutathione) were assayed by biochemical/enzyme-linked immunosorbent assay techniques in blood fractions.ResultsIn both trials, the nutriceutical induced significantly faster healing (P < 0.01-0.05) with reduced incidence of relapses (P < 0.05) as compared to control groups, which was confirmed by decreased viral load and increased antiviral cytokine and peroxynitrite plasma levels. Plasma antioxidant capacity was higher (P < 0.01) in the experimental versus control groups.ConclusionsResults document positive clinical outcomes of the selected nutriceutical associated with conventional protocols in the management of relapsing mucocutaneous human papillomavirus and herpes infections.