RESUMEN
BACKGROUND: The dietary model of metabolic syndrome has continued to aid our understanding of its pathogenesis and possible management interventions. However, despite progress in research, therapy continues to be challenging for humans; hence, the search for newer treatment and prevention options continues. OBJECTIVE: The objective of this study was to evaluate the impact of dietary CQ10 supplementation on metabolic, oxidative, and inflammatory markers in a diet-induced mouse model of metabolic syndrome. METHODS: Mouse groups were fed a Standard Diet (SD), High-Fat High-Sugar (HFHS) diet, and SD or HFHS diet (with incorporated CQ10) at 60 and 120 mg/kg of feed. At the completion of the study (8 weeks), blood glucose levels, Superoxide Dismutase (SOD) activity, plasma insulin, leptin, adiponectin, TNF-α, IL-10, serum lipid profile, and Lipid Peroxidation (LPO) levels were assessed. The liver was either homogenised for the assessment of antioxidant status or processed for general histology. RESULTS: Dietary CQ10 mitigated HFHS diet-induced weight gain, decreased glucose, insulin, and leptin levels, and increased adiponectin levels in mice. Coenzyme-Q10 improved the antioxidant status of the liver and blood in HFHS diet-fed mice while also decreasing lipid peroxidation. Lipid profile improved, level of TNF-α decreased, and IL-10 increased following CQ10 diet. A mitigation of HFHS diet-induced alteration in liver morphology was also observed with CQ10. CONCLUSION: Dietary CQ10 supplementation mitigates HFHS diet-induced changes in mice, possibly through its anti-oxidant, anti-lipaemic, and anti-inflammatory potential.
Asunto(s)
Antiinflamatorios , Antioxidantes , Coenzimas/administración & dosificación , Dieta Alta en Grasa/efectos adversos , Suplementos Dietéticos/efectos adversos , Síndrome Metabólico/tratamiento farmacológico , Adiponectina , Animales , Insulina , Interleucina-10 , Leptina , Lípidos , Ratones , Factor de Necrosis Tumoral alfa , Ubiquinona/análogos & derivadosRESUMEN
The molybdenum cofactor (Moco) is a 520-Da prosthetic group that is synthesized in all domains of life. In animals, four oxidases (among them sulfite oxidase) use Moco as a prosthetic group. Moco is essential in animals; humans with mutations in genes that encode Moco biosynthetic enzymes display lethal neurological and developmental defects. Moco supplementation seems a logical therapy; however, the instability of Moco has precluded biochemical and cell biological studies of Moco transport and bioavailability. The nematode Caenorhabditis elegans can take up Moco from its bacterial diet and transport it to cells and tissues that express Moco-requiring enzymes, suggesting a system for Moco uptake and distribution. Here we show that protein-bound Moco is the stable, bioavailable species of Moco taken up by C. elegans from its diet and is an effective dietary supplement, rescuing a Celegans model of Moco deficiency. We demonstrate that diverse Moco:protein complexes are stable and bioavailable, suggesting a new strategy for the production and delivery of therapeutically active Moco to treat human Moco deficiency.
Asunto(s)
Caenorhabditis elegans/metabolismo , Coenzimas/administración & dosificación , Errores Innatos del Metabolismo de los Metales/terapia , Metaloproteínas/administración & dosificación , Pteridinas/administración & dosificación , Animales , Bacterias/metabolismo , Transporte Biológico , Coenzimas/deficiencia , Coenzimas/farmacocinética , Humanos , Metaloproteínas/deficiencia , Metaloproteínas/farmacocinética , Cofactores de Molibdeno , Unión Proteica , Pteridinas/farmacocinéticaRESUMEN
Gyrate Atrophy (GA) of the choroid and retina (MIM# 258870) is an autosomal recessive disorder due to mutations of the OAT gene encoding ornithine-delta-aminotransferase (OAT), associated with progressive retinal deterioration and blindness. The disease has a theoretical global incidence of approximately 1:1,500,000. OAT is mainly involved in ornithine catabolism in adults, thus explaining the hyperornithinemia as hallmark of the disease. Patients are treated with an arginine-restricted diet, to limit ornithine load, or the administration of Vitamin B6, a precursor of the OAT coenzyme pyridoxal phosphate. Although the clinical and genetic aspects of GA are known for many years, the enzymatic phenotype of pathogenic variants and their response to Vitamin B6, as well as the molecular mechanisms explaining retinal damage, are poorly clarified. Herein, we provide an overview of the current knowledge on the biochemical properties of human OAT and on the molecular, cellular, and clinical aspects of GA.
Asunto(s)
Coenzimas/administración & dosificación , Atrofia Girata/dietoterapia , Atrofia Girata/enzimología , Ornitina-Oxo-Ácido Transaminasa/deficiencia , Fosfato de Piridoxal/administración & dosificación , Vitamina B 6/administración & dosificación , Arginina/metabolismo , Coroides/enzimología , Coroides/patología , Cromosomas Humanos Par 10 , Dieta/métodos , Expresión Génica , Atrofia Girata/genética , Atrofia Girata/patología , Humanos , Modelos Moleculares , Mutación , Ornitina/metabolismo , Ornitina-Oxo-Ácido Transaminasa/química , Ornitina-Oxo-Ácido Transaminasa/genética , Multimerización de Proteína , Estructura Secundaria de Proteína , Retina/enzimología , Retina/patologíaRESUMEN
A growing body of research has focused on modifiable risk factors for prevention and attenuation of cognitive decline in aging. This has led to an unprecedented interest in the relationship between diet and cognitive function. Several preclinical and epidemiologic studies suggest that dietary intervention can be used to improve cognitive function but randomized controlled trials are increasingly failing to replicate these findings. Here, we use a canine model of aging to evaluate the effects of specific components of diet supplementation which contain both antioxidants and a combination of mitochondrial cofactors (lipoic acid [LA] and acetyl-l-carnitine) on a battery of cognitive functions. Our data suggest that supplementation with mitochondrial cofactors, but not LA or antioxidant alone, selectively improve long-term recall in aged canines. Furthermore, we found evidence that LA alone could have cognitive impairing effects. These results contrast to those of a previous longitudinal study in aged canine. Our data demonstrate that one reason for this difference may be the nutritional status of animals at baseline for the 2 studies. Overall, this study suggests that social, cognitive, and physical activity together with optimal dietary intake (rather than diet alone) promotes successful brain aging.
Asunto(s)
Acetilcarnitina/administración & dosificación , Envejecimiento/psicología , Antioxidantes/administración & dosificación , Coenzimas/administración & dosificación , Trastornos del Conocimiento/dietoterapia , Trastornos del Conocimiento/prevención & control , Cognición/efectos de los fármacos , Cognición/fisiología , Suplementos Dietéticos , Ácido Tióctico/administración & dosificación , Acetilcarnitina/farmacología , Fenómenos Fisiológicos Nutricionales de los Animales/fisiología , Animales , Antioxidantes/farmacología , Coenzimas/farmacología , Trastornos del Conocimiento/psicología , Modelos Animales de Enfermedad , Perros , Femenino , Masculino , Memoria a Largo Plazo/efectos de los fármacos , Ácido Tióctico/farmacologíaRESUMEN
OBJECTIVE: To investigate the effect of coenzyme complex on decreasing cardiotoxicity in elderly patients with gastrointestinal cancer who were treated by chemotherapy. METHODS: From September 2011 to February 2015, we recruited 54 elderly (with more than 70 years of age) patients with gastrointestinal cancer, with advanced disease. Then treated with chemotherapy combined with or without coenzyme complex. After two cycles of treatment, the effect of coenzyme complex on decreasing cardiotoxicity were evaluated. RESULTS: Chemotherapy was combined with coenzyme complex in 32 patients (22man, 10 woman; median age: 74 years, range: 70-87 years) without coenzyme complex in 22 patients (15man, 7 woman; median age: 73 years, range: 70-80 years) with gastrointestinal cancer. Cardiac event was significantly lower in patients treated with chemotherapy combined with coenzyme complex (p<0.01). CONCLUSIONS: Coenzyme Complex decreased cardiotoxicity when combined with chemotherapy in treating elderly patients with gastrointestinal cancer.
Asunto(s)
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapéutico , Cardiotoxicidad/prevención & control , Coenzimas/administración & dosificación , Neoplasias Gastrointestinales/complicaciones , Neoplasias Gastrointestinales/terapia , Anciano , Anciano de 80 o más Años , Cardiotoxicidad/etiología , Terapia Combinada , Femenino , Estudios de Seguimiento , Neoplasias Gastrointestinales/tratamiento farmacológico , Neoplasias Gastrointestinales/patología , Humanos , Masculino , Estadificación de Neoplasias , PronósticoRESUMEN
BACKGROUND: A significant association between Zn and Se homeostasis exists. At the same time, data on the influence of zinc supplementation on selenium distribution in organs and tissues seem to be absent. Therefore, the primary objective of the current study is to investigate the influence of zinc asparaginate supplementation on zinc and selenium distribution and serum superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity in Wistar rats. METHODS: 36 rats were used in the experiment. The duration of the experiment was 7 and 14 days in the first and second series, respectively. The rats in Group I were used as the control ones. Animals in Groups II and III daily obtained zinc asparaginate (ZnA) in the doses of 5 and 15 mg/kg weight, respectively. Zinc and selenium content in liver, kidneys, heart, muscle, serum and hair was assessed using inductively coupled plasma mass spectrometry. Serum SOD and GPx activity was analysed spectrophotometrically using Randox kits. RESULTS: Intragastric administration of zinc asparaginate significantly increased liver, kidney, and serum zinc content without affecting skeletal and cardiac muscle levels. Zinc supplementation also stimulated selenium retention in the rats' organs. Moreover, a significant positive correlation between zinc and selenium content was observed. Finally, zinc asparaginate treatment has been shown to modulate serum GPx but not SOD activity. CONCLUSIONS: The obtained data indicate that zinc-induced increase in GPx activity may be mediated through modulation of selenium status. However, future studies are required to estimate the exact mechanisms of zinc and selenium interplay.
Asunto(s)
Suplementos Dietéticos , Glutatión Peroxidasa/sangre , Riñón/metabolismo , Hígado/metabolismo , Oxidorreductasas/sangre , Selenio/metabolismo , Zinc/administración & dosificación , Animales , Asparagina/administración & dosificación , Coenzimas/administración & dosificación , Coenzimas/sangre , Coenzimas/metabolismo , Glutatión Peroxidasa/química , Masculino , Estado Nutricional , Ratas Sprague-Dawley , Espectrofotometría Atómica , Superóxido Dismutasa/sangre , Factores de Tiempo , Distribución Tisular , Zinc/sangre , Zinc/metabolismoAsunto(s)
Antineoplásicos/efectos adversos , Asparaginasa/efectos adversos , Enfermedad Hepática Inducida por Sustancias y Drogas/tratamiento farmacológico , Coenzimas/uso terapéutico , Antineoplásicos/administración & dosificación , Antineoplásicos/uso terapéutico , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapéutico , Asparaginasa/administración & dosificación , Asparaginasa/uso terapéutico , Enfermedad Hepática Inducida por Sustancias y Drogas/diagnóstico , Coenzimas/administración & dosificación , Resultado Fatal , Femenino , Humanos , Hígado/metabolismo , Hígado/patología , Masculino , Persona de Mediana Edad , Leucemia-Linfoma Linfoblástico de Células Precursoras/complicaciones , Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamiento farmacológico , Resultado del TratamientoRESUMEN
BACKGROUND: Phenylketonuria (PKU) is an autosomal recessive inherited disease associated with impaired metabolism of the amino acids phenylalanine (Phe) and tyrosine. The main criterion for diagnosis of PKU is high blood Phe level determined during neonatal screening. In case where PKU patient is responsive to tetrahydrobiopterin treatment, sapropterin restores the impaired activity of the enzyme phenylalanine hydroxylase, resulting in the stimulation of normal Phe metabolism and thereby enhancing patient tolerance to natural products. AIM: The present open, non-comparative clinical study was initiated to assess the degree and frequency of response after 8-day sapropterin administration and assess the safety of 6-week sapropterin treatment in patients with PKU and hyperphenylalaninemia. PATIENTS AND METHODS: The study enrolled 90 patients with PKU. The criterion of response to 8-day sapropterin therapy was the reduction of Phe blood levels ≥ 30% compared with the baseline value. RESULTS: Positive response to treatment was observed in 30 (33.3%) patients (95% CI 23.7-44.1). The mean percentage change in Phe blood levels after the 8-day response test period compared to Phe levels prior to dosing was 14.1 ± 28.4% in the overall subject population (95% CI 8.2-20.1) and 44.3 ± 15.1% in the subpopulation of patients with a positive response (95% CI 38.6-49.9). During the study, adverse events were reported in 24 (26.7%) patients in the overall population in 16 (53.3%) patients in the subpopulation who had a response. CONCLUSION: The study results confirmed the efficacy and safety of sapropterin therapy in patients with PKU, which is consistent with international clinical trials data.
Asunto(s)
Biopterinas/análogos & derivados , Fenilalanina/sangre , Fenilcetonurias , Adolescente , Biopterinas/administración & dosificación , Biopterinas/efectos adversos , Niño , Preescolar , Coenzimas/administración & dosificación , Coenzimas/efectos adversos , Dihidropteridina Reductasa/metabolismo , Monitoreo de Drogas/métodos , Femenino , Humanos , Recién Nacido , Masculino , Tamizaje Neonatal/métodos , Fenilalanina Hidroxilasa/metabolismo , Fenilcetonurias/sangre , Fenilcetonurias/tratamiento farmacológico , Fenilcetonurias/fisiopatología , Índice de Severidad de la Enfermedad , Resultado del TratamientoRESUMEN
Three of our research efforts are reviewed, which suggest that optimizing metabolism will delay aging and the diseases of aging in humans. (1) Research on delay of the mitochondrial decay of aging by supplementing rats with lipoic acid and acetyl carnitine. (2) The triage theory, which posits that modest micronutrient deficiencies (common in much of the population) accelerate molecular aging, including mitochondrial decay, and supportive evidence, including an analysis in depth of vitamin K, that suggests the importance of achieving optimal micronutrient intake for longevity. (3) The finding that decreased enzyme binding constants (increased Km) for coenzymes (or substrates) can result from protein deformation and loss of function due to loss of membrane fluidity with age, or to polymorphisms or mutation. The loss of enzyme function can be ameliorated by high doses of a B vitamin, which raises coenzyme levels, and indicates the importance of understanding the effects of age, or polymorphisms, on micronutrient requirements.
Asunto(s)
Envejecimiento/metabolismo , Senescencia Celular/efectos de los fármacos , Suplementos Dietéticos , Micronutrientes/administración & dosificación , Mitocondrias/efectos de los fármacos , Enfermedades Mitocondriales/prevención & control , Acetilcarnitina/administración & dosificación , Factores de Edad , Envejecimiento/patología , Animales , Coenzimas/administración & dosificación , Enzimas/metabolismo , Humanos , Longevidad , Micronutrientes/deficiencia , Micronutrientes/metabolismo , Mitocondrias/enzimología , Mitocondrias/patología , Enfermedades Mitocondriales/enzimología , Enfermedades Mitocondriales/patología , Ácido Tióctico/administración & dosificación , Vitamina K/administración & dosificaciónRESUMEN
A UPLC-MS method for determining Coenzyme Q(10) (CoQ(10)) levels in rat serum was developed. CoQ(10) was quantitatively extracted into 2-propanol using a fast extraction procedure. The separation of CoQ(10) was performed on a Waters Acquity UPLCtrade mark BEH C(18) column (1.7 microm, 1.0 mm x 50 mm) with the mobile phase containing acetonitrile, 2-propanol, and formic acid (90:10:0.1) over 5 min. The sensitivity of this method allows for the quantitation of 50 ng/mL CoQ(10) in serum (S/N=10). The linearity of this method was found to be from 50 to 20,000 ng/mL. The precision was less than 10% (intra- and inter-day), and the average extraction recovery was between 90 and 105%. This procedure provides a precise, sensitive and direct assay method for the determination of CoQ(10) in rat serum after oral administration. This method could be applied to further pharmacokinetic studies of CoQ(10).
Asunto(s)
Cromatografía Liquida/métodos , Espectrometría de Masas/métodos , Ubiquinona/análogos & derivados , 2-Propanol/química , Acetatos/química , Ácido Acético/química , Acetonitrilos/química , Administración Oral , Hidróxido de Amonio , Animales , Área Bajo la Curva , Coenzimas/administración & dosificación , Coenzimas/sangre , Coenzimas/farmacocinética , Formiatos/química , Hidróxidos/química , Modelos Lineales , Tasa de Depuración Metabólica , Ratas , Ratas Sprague-Dawley , Reproducibilidad de los Resultados , Solventes/química , Ubiquinona/administración & dosificación , Ubiquinona/análisis , Ubiquinona/sangre , Ubiquinona/farmacocinética , Ubiquinona/normasRESUMEN
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.
Asunto(s)
Ubiquinona/análogos & derivados , alfa-Tocoferol/farmacocinética , Adulto , Disponibilidad Biológica , Coenzimas/administración & dosificación , Coenzimas/sangre , Coenzimas/farmacocinética , Estudios Cruzados , Femenino , Humanos , Absorción Intestinal , Masculino , Ubiquinona/administración & dosificación , Ubiquinona/sangre , Ubiquinona/farmacocinética , alfa-Tocoferol/administración & dosificación , alfa-Tocoferol/sangreRESUMEN
This study investigates aging-related changes in lipid peroxidation and functionality in liver and skeletal-muscle mitochondria in rats fed a diet rich in polyunsaturated fatty acids (PUFA), depending on supplementation or not with coenzyme Q(10) (CoQ(10)). Two groups of rats were fed for 24 months on a PUFA-rich diet, differing in supplementation or not with CoQ(10). At 6 and 24 months mitochondria were analyzed for fatty acid profile; hydroperoxides; alpha-tocopherol; CoQ(9;) CoQ(10;) cytochromes b, c+c(1), and a+a(3) contents; cytochrome c oxidase activity; and catalase activity in cytosol. Results of this study showed for the supplemented group an age-associated decrease in the peroxidizability index, an increase in catalase activity in skeletal muscle, and modulation of the aging-related changes in different mitochondrial electron-transport-chain components in skeletal muscle. These findings provide mechanisms to explain the effect of CoQ(10) in extending the life span of animals fed a PUFA-rich diet.
Asunto(s)
Envejecimiento/efectos de los fármacos , Envejecimiento/metabolismo , Ácidos Grasos Insaturados/administración & dosificación , Mitocondrias Hepáticas/efectos de los fármacos , Mitocondrias Hepáticas/metabolismo , Mitocondrias Musculares/metabolismo , Músculo Esquelético/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Ubiquinona/análogos & derivados , Animales , Catalasa/metabolismo , Coenzimas/administración & dosificación , Coenzimas/farmacología , Grasas Insaturadas en la Dieta/administración & dosificación , Complejo IV de Transporte de Electrones/metabolismo , Peroxidación de Lípido , Masculino , Ratas , Ratas Wistar , Ubiquinona/administración & dosificación , Ubiquinona/farmacología , alfa-Tocoferol/metabolismoAsunto(s)
Cardiomiopatías/inducido químicamente , Inhibidores de Hidroximetilglutaril-CoA Reductasas/efectos adversos , Ubiquinona/análogos & derivados , Cardiomiopatías/tratamiento farmacológico , Cardiomiopatías/fisiopatología , Coenzimas/administración & dosificación , Coenzimas/deficiencia , Coenzimas/fisiología , Humanos , Inhibidores de Hidroximetilglutaril-CoA Reductasas/administración & dosificación , Efecto Placebo , Resultado del Tratamiento , Ubiquinona/administración & dosificación , Ubiquinona/deficiencia , Ubiquinona/fisiologíaRESUMEN
As part of a safety evaluation of Coenzyme Q10, a subchronic toxicology study was conducted. Coenzyme Q10 was repeatedly administered orally to male and female Crl:CD(SD) rats at daily dose levels of 300, 600 and 1200 mg/kg for 13 weeks. Neither death nor any toxicological signs were observed in any group during the administration period. No change related to the test substance administered was observed in any group with regard to body weight, food consumption, ophthalmoscopy, hematology, blood biochemistry, necropsy, organ weights or histopathology. Based on these results, the non-observed-adverse-effect level (NOAEL) of Coenzyme Q10 was considered to be 1200 mg/kg/day for male and female rats under these study conditions.
Asunto(s)
Suplementos Dietéticos/toxicidad , Pruebas de Toxicidad Crónica , Ubiquinona/análogos & derivados , Administración Oral , Animales , Peso Corporal/efectos de los fármacos , Coenzimas/administración & dosificación , Coenzimas/toxicidad , Conducta Alimentaria/efectos de los fármacos , Femenino , Masculino , Nivel sin Efectos Adversos Observados , Tamaño de los Órganos/efectos de los fármacos , Especificidad de Órganos , Ratas , Ratas Sprague-Dawley , Ubiquinona/administración & dosificación , Ubiquinona/toxicidadAsunto(s)
Ubiquinona/análogos & derivados , Administración Oral , Adulto , Área Bajo la Curva , Dolor de Espalda/inducido químicamente , Disponibilidad Biológica , Cápsulas , Coenzimas/administración & dosificación , Coenzimas/farmacocinética , Estudios Cruzados , Método Doble Ciego , Femenino , Gelatina/química , Cefalea/inducido químicamente , Humanos , Masculino , Prurito/inducido químicamente , Factores Sexuales , Sinusitis/inducido químicamente , Factores de Tiempo , Ubiquinona/administración & dosificación , Ubiquinona/farmacocinética , Vitaminas/administración & dosificación , Vitaminas/efectos adversos , Vitaminas/farmacocinéticaRESUMEN
Coenzyme Q10 (CoQ10) is widely consumed as a food supplement because of its recognition as an important nutrient in supporting human health. Absorption of compounds from the gastrointestinal tract is one of the important determinants of oral bioavailability. However, the absorption of dietary CoQ10 is slow and limited due to its hydrophobicity and large molecular weight. The absorption of orally applied compounds can be enhanced by interactions with food or food components. Thus, we investigated the effect of food intake on the absorption of CoQ10 after oral supplementation. In this study, we demonstrated that food intake enhanced the intestinal absorption of CoQ10. In order to improve intestinal absorption of CoQ10 after oral supplementation, we developed an emulsion formulation. Intestinal absorption of CoQ10 after administration of the emulsion formulation was also enhanced by food intake. Moreover, the peak concentration and the extent of absorption after administration of the emulsion formulation were greater than those after administration of a suspension formulation. It is possible that administration of CoQ10 in an emulsion formulation enhances the pharmacological effects of CoQ10.
Asunto(s)
Ingestión de Alimentos/fisiología , Absorción Intestinal , Ubiquinona/análogos & derivados , Administración Oral , Animales , Disponibilidad Biológica , Coenzimas/administración & dosificación , Coenzimas/farmacocinética , Emulsiones , Masculino , Peso Molecular , Ratas , Ratas Wistar , Ubiquinona/administración & dosificación , Ubiquinona/farmacocinéticaRESUMEN
Recent studies support a role for excitotoxicity in the development of retinal ganglion cell (RGC) damage in subjects suffering from glaucoma. Coenzyme Q10 (CoQ10), an essential cofactor of the electron transport chain, has been reported to afford neuroprotection, preventing the formation of the mitochondrial permeability transition pore. Using an established animal model of retinal ischemia/reperfusion here, we show that synaptic glutamate increases at 130min from beginning of reperfusion and delayed apoptosis in the RGC layer is seen at 24h. Intraocular administration of CoQ10 minimizes glutamate increase and affords neuroprotection, suggesting that oxidative stress and energy failure might be implicated in the mechanisms of RGC death.
Asunto(s)
Presión Intraocular/fisiología , Isquemia/patología , Enfermedades de la Retina/prevención & control , Ubiquinona/análogos & derivados , Administración Tópica , Animales , Coenzimas/administración & dosificación , Coenzimas/uso terapéutico , Ácido Glutámico/toxicidad , Etiquetado Corte-Fin in Situ , Masculino , Microdiálisis , Ratas , Ratas Wistar , Enfermedades de la Retina/patología , Células Ganglionares de la Retina/efectos de los fármacos , Células Ganglionares de la Retina/patología , Ubiquinona/administración & dosificación , Ubiquinona/uso terapéuticoRESUMEN
In present research the action of coenzyme Q10 on energetic metabolism and antioxidant system at different temperature conditions has been studied. It was established that the addition of coenzyme Q10 caused inadequate stimulation of main metabolic systems that could lead to running out of functional reserves of cardiomyocytes. The use of coenzyme Q10 helped to optimize intracellular compensating mechanisms supplying the defense of myocardium. Introduction in a diet coenzyme Q10 in conditions of a temperature's comfort threshold excess and development of a histic hypoxia can promote the decrease of gravity of hypoxic myocardium's lesions and to glycogenolysis' amplification that promotes maintenance of an energy homeostasis of a myocardium in posthypoxia term. It is possible to assume, that the augmentation of duration of reception coenzyme Q10 or its dosages can render more expressed protective effect.
Asunto(s)
Adaptación Fisiológica , Suplementos Dietéticos , Metabolismo Energético/efectos de los fármacos , Hipoxia , Miocardio , Ubiquinona/análogos & derivados , Animales , Coenzimas/administración & dosificación , Coenzimas/farmacología , Modelos Animales de Enfermedad , Vivienda para Animales , Hipoxia/metabolismo , Hipoxia/fisiopatología , Masculino , Miocardio/enzimología , Miocardio/metabolismo , Ratas , Temperatura , Ubiquinona/administración & dosificación , Ubiquinona/farmacologíaRESUMEN
Hypertension is the most common reason for visits to physicians' offices and the primary reason for prescription drug use. The target organ damage associated with hypertension, such as stroke, myocardial infarction, congestive heart failure, renal disease and large artery disease, can be mitigated by aggressive nondrug and drug therapies. Hypertension is a syndrome of various metabolic, functional and structural abnormalities that must be viewed in a more global setting of cardiovascular risk. Aggressive detection, evaluation and treatment of the 'blood vessel health' is mandatory to modern hypertensive care. Lifestyle modifications in conjunction with vitamins, minerals, antioxidants, nutraceutical supplements, optimal nutrition and drug therapy will prevent and treat hypertension and its sequelae while addressing global cardiovascular risk, vascular biology, endothelial dysfunction and overall vascular health.
Asunto(s)
Suplementos Dietéticos , Hipertensión/terapia , Calcio/administración & dosificación , Coenzimas/administración & dosificación , Comorbilidad , Endotelio Vascular , Ajo , Humanos , Hipertensión/tratamiento farmacológico , Hipertensión/epidemiología , Hipertensión/prevención & control , Estilo de Vida , Magnesio/administración & dosificación , Estrés Oxidativo , Potasio/administración & dosificación , Potasio/efectos adversos , Cloruro de Sodio/administración & dosificación , Cloruro de Sodio/efectos adversos , Ubiquinona/administración & dosificación , Ubiquinona/análogos & derivadosRESUMEN
Coenzyme Q10 (CoQ10) is a lipid-soluble antioxidant and essential component of the mitochondrial electron transfer system in the body, and is in wide use as a functional food material and cosmetic raw material. However, as CoQ10 is extremely lipid-soluble, absorption by the body is not easy. In general, people use soft-gel capsules in which CoQ10 is suspended in oil, and take these capsules with food. PureSorb-Q40 (P40) was developed to improve CoQ10 processability and absorption when taken without food, and the present study compared the effects of food on absorption between P40 and conventional lipid-soluble CoQ10 in rats and humans. The results of a rat study showed higher uptake when P40 was administered in the fasting state or with food compared to lipid-soluble CoQ10. The results of a human study showed that uptake was favorable when P40 was administered in the fasting state, and even when administered postprandially, a significant difference was noted in uptake rate up to 6 h after intake and uptake volume up to 8 h after intake when compared to lipid-soluble CoQ10. These results show that any CoQ10 product using P40 can be quickly and reliably absorbed by the body regardless of dosage form or intake time.