ubiquinone and Vitamin-A-Deficiency

The fruit of the oil palm tree (Elaeis guineesis) is the source of antioxidant-rich red palm oil. Red palm oil is a rich source of phytonutrients such as tocotrienols, tocopherols, carotenoids, phytosterols, squalene, and coenzyme Q10, all of which exhibit nutritional properties and oxidative stability. Mutagenic, nutritional, and toxicological studies have shown that red palm oil contains highly bioavailable β-carotene and vitamin A and is reasonably stable to heat without any adverse effects. This review provides a comprehensive overview of the nutritional properties of red palm oil. The possible antiatherogenic, antihemorrhagic, antihypertensive, anticancer, and anti-infective properties of red palm oil are examined. Moreover, evidence supporting the potential effectiveness of red palm oil to overcome vitamin A deficiency in children and pregnant women, to improve ocular complications of vitamin A deficiency, to protect against ischemic heart disease, to promote normal reproduction in males and females, to aid in the management of diabetes, to ameliorate the adverse effects of chemotherapy, and to aid in managing hypobaric conditions is presented.

Topics: Animals; Antioxidants; Cardiovascular Diseases; Carotenoids; Disease Models, Animal; Evidence-Based Medicine; Fruit; Health Promotion; Humans; Palm Oil; Phytochemicals; Randomized Controlled Trials as Topic; Recommended Dietary Allowances; Squalene; Ubiquinone; Vitamin A Deficiency; Vitamin E

Topics: Animals; Cattle; Electron Transport; Hormones; Mitochondria, Liver; NAD; Neoplasms; Photosynthesis; Rats; Succinate Dehydrogenase; Ubiquinone; Vitamin A Deficiency; Vitamin E Deficiency

Topics: Animals; Carbon Isotopes; Cats; Cattle; Esterases; Female; Humans; Kidney; Male; Oxidation-Reduction; Oxidative Phosphorylation; Phosphoric Monoester Hydrolases; Pregnancy; Rabbits; Rats; Renal Aminoacidurias; Swine; Transaminases; Turkeys; Ubiquinone; Vitamin A; Vitamin A Deficiency; Vitamin E; Vitamin E Deficiency

Despite supplementation with standard multivitamins and pancreatic enzymes, deficiencies of vitamins D and K and antioxidants are common in cystic fibrosis (CF).. In this non-randomized, open-label study, AquADEKs® softgels were given daily over 12 weeks to 14 CF subjects (mean age 15 years, range 10-23) without a preceding wash-out period. Both pancreatic sufficient and insufficient subjects were enrolled. Plasma vitamin and antioxidant levels, urine 8-isoprostane levels, anthropometric measures, and pulmonary function were determined at baseline, 6 and 12 weeks.. Daily supplementation significantly increased plasma beta(β)-carotene, coenzyme Q10, and γ-tocopherol concentrations, decreased proteins induced in vitamin K absence (PIVKA-II) levels, but did not normalize vitamin D and K status in all subjects. Vitamin A levels did not exceed the normal range for any subject during the entire study period. Modest improvements in weight percentile and pulmonary function were observed. Change in plasma β-carotene concentrations weakly correlated with changes in weight and body mass index percentiles.. In this study, AquADEKs® increased systemic antioxidant levels, while maintaining vitamin A levels in the normal range, and improved but did not completely normalize vitamin D and K status. Increased β-carotene levels were associated with improved growth parameters. These results warrant further clinical evaluation in CF.

Topics: Adolescent; Antioxidants; Biomarkers, Pharmacological; Body Mass Index; Child; Cystic Fibrosis; Dietary Supplements; Dinoprost; Exocrine Pancreatic Insufficiency; Female; Humans; Male; Oxidative Stress; Respiratory Function Tests; Treatment Outcome; Ubiquinone; Vitamin A Deficiency; Vitamin D Deficiency; Vitamin K Deficiency; Vitamins; Young Adult

Male and female C57B1/6 mice were rendered vitamin A-deficient, and the effects of this deficiency on certain xenobiotic-metabolizing enzymes and defenses against oxidative stress were examined. Vitamin A deficiency significantly increased the levels of DT-diaphorase, glutathione transferase, and catalase in the hepatic cytosolic fraction from male mice (5.2-, 1.6-, and 3.5-fold, respectively), as well as from female mice (4.8-, 3.3-, and 2.4-fold, respectively). In the hepatic mitochondrial fraction (containing peroxisomes) from male animals, the activities of urate oxidase and catalase were increased 3.4- and 1.7-fold, respectively. The activity of catalase in the mitochondrial fraction from female mice was not affected by vitamin A deficiency, whereas the activity of peroxisomal urate oxidase was increased 2.9-fold. The hepatic level of ubiquinone was increased somewhat. The significance of the increases observed here is presently unclear, but it may be speculated that vitamin A and/or its metabolites are somehow involved in the down-regulation of these proteins. Another possibility is that these enzymes are increased as a result of hepatic oxidative stress caused by vitamin A deficiency. However, vitamin A deficiency had no effect on the activity of superoxide dismutase in this study, whereas the activity of glutathione peroxidase was slightly decreased (27%) in the hepatic cytosolic fraction from male mice. In addition, the hepatic level of alpha-tocopherol was decreased dramatically in the vitamin A-deficient animals.

Topics: Animals; Antioxidants; Female; Liver; Male; Mice; Mice, Inbred C57BL; Organ Size; Oxidative Stress; Sex Characteristics; Ubiquinone; Vitamin A Deficiency; Vitamin E; Xenobiotics

The aim of this study was to investigate comparative effects of vitamin A deficiency on respiratory activity and structural integrity in liver and heart mitochondria. Male rats were fed a liquid control diet (control rats) or a liquid vitamin A-deficient diet (vitamin A-deficient rats) for 50 days. One group of vitamin-A deficient rats was refed a control diet for 15 days (vitamin A-recovered rats). To assess the respiratory function of mitochondria the contents of coenzyme Q (ubiquinone, CoQ), cytochrome c and the activities of the whole electron transport chain and of each of its respiratory complexes were evaluated. Chronic vitamin A deficiency promoted a significant increase in the endogenous coenzyme Q content in liver and heart mitochondria when compared with control values. Vitamin A deficiency induced a decrease in the activity of complex I (NADH-CoQ reductase) and complex II (succinate-CoQ reductase) and in the levels of complex I and cytochrome c in heart mitochondria. However, NADH and succinate oxidation rates were maintained at the control levels due to an increase in the CoQ content in accordance with the kinetic behaviour of CoQ as an homogeneous pool. On the contrary, the high CoQ content did not affect the electron-transfer rate in liver mitochondria, whose integrity was preserved from the deleterious effects of the vitamin A deficiency. Ultrastructural assessment of liver and heart showed that vitamin A deficiency did not induce appreciable alterations in the morphology of their mitochondria. After refeeding the control diet, serum retinol, liver and heart CoQ content and the activity of complex I and complex II in heart mitochondria returned to normality. However, the activities of both whole electron transfer chain and complex I in liver were increased over the control values. The interrelationships between physiological antioxidants in biological membranes and the beneficial effects of their administration in mitochondrial diseases are discussed.

Topics: Animals; Cytochrome c Group; Electron Transport; Male; Mitochondria, Heart; Mitochondria, Liver; Rats; Retinoids; Ubiquinone; Vitamin A Deficiency; Vitamin E

Defects of NADH:coenzyme Q oxidoreductase (complex I) of mitochondria have been described in many congenital and acquired diseases. Administration of coenzyme Q (CoQ, ubiquinone) has been shown to benefit patients with some of these diseases. However, the mechanisms by which CoQ exerts the therapeutic effects are not clearly understood. A reason could be the lack of saturation of CoQ, in kinetic terms, for complex I activity. However, this hypothesis has not been proved in vivo because of the difficulty to incorporate CoQ into the mitochondrial membranes. We have found a deficiency in respiratory complex I in heart mitochondria from vitamin A-deficient rats which was accompanied by high CoQ content. The defect in complex I activity was compensated by the increase in CoQ to maintain the mitochondrial electron transfer rate. This finding supports, for the first time in an in vivo experimental approach, the kinetic hypothesis to explain the short-term therapeutic effects of CoQ.

Topics: Animals; Electron Transport Complex I; Kinetics; Mitochondria, Heart; NADH, NADPH Oxidoreductases; Rats; Ubiquinone; Vitamin A Deficiency

Topics: Animals; Biological Transport; Carbon Isotopes; Chromatography; Enzyme Activation; Intestinal Absorption; Rats; Ubiquinone; Vitamin A; Vitamin A Deficiency

Topics: Animals; Carbon Isotopes; Carotenoids; Female; Liver; Male; Mevalonic Acid; Rats; Time Factors; Ubiquinone; Vitamin A; Vitamin A Deficiency

Topics: Alkalies; Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Chemical Precipitation; Chromatography; Guinea Pigs; Injections, Intraperitoneal; Kidney; Liver; Male; Rats; Solvents; Spectrophotometry; Sterols; Ubiquinone; Vitamin A; Vitamin A Deficiency

Topics: Animals; Body Weight; Cecum; Female; Gastric Mucosa; Intestinal Mucosa; Kidney; Liver; Male; Rats; Ubiquinone; Vaginal Smears; Vitamin A; Vitamin A Deficiency

Topics: Adolescent; Aged; Avitaminosis; Congenital Abnormalities; Diet Fads; Drug Therapy; Electron Transport; Folic Acid Deficiency; History, 20th Century; Humans; Middle Aged; Nutrition Surveys; Oxidative Phosphorylation; Psychology, Adolescent; Riboflavin Deficiency; Ubiquinone; United States; Vitamin A Deficiency

Topics: Animals; Benzopyrans; In Vitro Techniques; Intestinal Mucosa; Kidney; Liver; Mevalonic Acid; Rats; Ubiquinone; Vitamin A Deficiency

Topics: Carbon Isotopes; Chromans; Intestine, Small; Intestines; Kidney; Liver; Metabolism; Protein Deficiency; Rats; Research; Ubiquinone; Vitamin A Deficiency

Topics: Liver; Phenylalanine; Research; Ubiquinone; Vitamin A; Vitamin A Deficiency; Vitamin E

1. Vitamin A-deficient rats were compared with similar animals given small amounts of vitamin A sufficient for adequate growth and with animals given large amounts of vitamin A. The effects of pair-feeding and feeding ad libitum were compared. 2. Ubiquinone and cholesterol concentrations in liver were measured at various stages of the deficiency, and the uptake of radioactive mevalonate and acetate into isoprenoid compounds was studied. 3. Ubiquinone concentrations in liver increased markedly in deficient rats compared with adequate controls, and heavy vitamin A supplementation had a further effect in depressing ubiquinone concentrations. These effects were unrelated to food intake or to the size of the organs. 4. Radioactive uptake into ubiquinone was often greater in deficient livers, especially during the early stages of the experiments, but the effect was not consistent. 5. Cholesterol concentrations were usually higher in deficient livers and these were more affected by the feeding regimen. 6. No consistent effect of vitamin A deficiency or of vitamin A dosage on the incorporation of mevalonate into cholesterol or squalene was found. 7. No evidence has been found for a specific effect of vitamin A on isoprenoid synthesis at the metabolic level.

Topics: Acetates; Animals; Cholesterol; Liver; Metabolism; Mevalonic Acid; Pharmacology; Rats; Research; Squalene; Ubiquinone; Vitamin A; Vitamin A Deficiency

Topics: Animals; Blood; Blood Protein Electrophoresis; Cholesterol; Eye; Growth; Hematocrit; Hemoglobins; Liver; Rats; Serum Albumin; Serum Globulins; Ubiquinone; Vitamin A; Vitamin A Deficiency; Vitamin E

Topics: Cortisone; Liver; Metabolism; Pharmacology; Rats; Research; Ubiquinone; Vitamin A; Vitamin A Deficiency

Topics: Aging; Avitaminosis; Liver; Metabolism; Mitochondria; Rats; Research; Ubiquinone; Vitamin A Deficiency

Topics: Animals; Ascorbic Acid; Ascorbic Acid Deficiency; In Vitro Techniques; Liver; Mevalonic Acid; Rats; Squalene; Ubiquinone; Vitamin A Deficiency

Topics: Animals; Diet; Liver; Nutrition Assessment; Quinones; Rats; Steroids; Sterols; Tocopherols; Ubiquinone; Vitamin A; Vitamin A Deficiency; Vitamin E

Topics: Animals; Coenzymes; Diet; Lipid Metabolism; Lipids; Liver; Nutrition Assessment; Quinones; Rats; Ubiquinone; Vitamin A; Vitamin A Deficiency

Topics: Liver; Quinones; Time Factors; Ubiquinone; Vitamin A Deficiency

Topics: Adrenalectomy; Liver; Quinones; Ubiquinone; Vitamin A Deficiency