ABSTRACT
INTRODUCTION: Diabetes mellitus (T2DM) and cardiovascular diseases (CVDs) have become some of the most urgent and prevalent health problems in recent decades, side by side with the growing obesity crisis. The close relationship between T2DM and CVD has become clear: endothelial dysfunction caused by oxidative stress and inflammation resulting from hyperglycaemia are the key factors in the development of vascular complications of T2DM, leading to CVD. Coenzyme Q10 (CoQ10) is a great candidate for the treatment of these diseases, acting precisely at the intersection between T2DM and CVD that is oxidative stress, due to its strong antioxidant activity and fundamental physiological role in mitochondrial bioenergetics. CoQ10 is a biologically active liposoluble compound comprising a quinone group and a side chain of 10 isoprenoid units, which is synthesized endogenously in the body from tyrosine and mevalonic acid. The main biochemical action of CoQ10 is as a cofactor in the electron transport chain that synthesizes adenosine triphosphate (ATP). As most cellular functions depend on an adequate supply of ATP, CoQ10 is essential for the health of virtually all human tissues and organs. CoQ10 supplementation has been used as an intensifier of mitochondrial function and an antioxidant with the aim of palliating or reducing oxidative damage that can worsen the physiological outcome of a wide range of diseases including T2DM and CVDs. CONCLUSION: Although there is not enough evidence to conclude it is effective for different therapeutic indications, CoQ10 supplementation is probably safe and well-tolerated, with few drug interactions and minor side effects. Many valuable advances have been made in the use of CoQ10 in clinical practice for patients with T2DM and a high risk of CVD. However, further research is needed to assess the real safety and benefit to indicate CoQ10 supplementation in patients with T2DM.
Subject(s)
Cardiovascular Diseases , Diabetes Mellitus, Type 2 , Humans , Cardiovascular Diseases/drug therapy , Ubiquinone/therapeutic use , Antioxidants/therapeutic use , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/drug therapy , Adenosine TriphosphateABSTRACT
Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy specific liver disease characterized by pruritus, elevated serum bile acids and abnormal liver function that may be associated with severe adverse pregnancy outcomes. We previously reported that plasma coenzyme Q10 (CoQ10) is decreased in women with ICP as it is its analogue coenzyme Q9 (CoQ9) in rats with ethinyl estradiol (EE)-induced cholestasis. The aim of the present study was to evaluate the possible therapeutic role of CoQ10 in experimental hepatocellular cholestasis and to compare it with ursodeoxycholic acid (UDCA) supplementation. Bile acids, CoQ9, CoQ10, transaminases, alkaline phosphatase, retinol, α-tocopherol, ascorbic acid, thiobarbituric acid reactive substances, carbonyls, glutathione, superoxide dismutase and catalase were assessed in plasma, liver and/or hepatic mitochondria in control and cholestatic rats supplemented with CoQ10 (250 mg/kg) administered alone or combined with UDCA (25 mg/kg). CoQ10 supplementation prevented bile flow decline (P < 0.05) and the increase in serum alkaline phosphatase and bile acids, particularly lithocholic acid (P < 0.05) in cholestatic rats. Furthermore, it also improved oxidative stress parameters in the liver, increased both CoQ10 and CoQ9 plasma levels and partially prevented the fall in α-tocopherol (P < 0.05). UDCA also prevented cholestasis, but it was less efficient than CoQ10 to improve the liver redox environment. Combined administration of CoQ10 and UDCA resulted in additive effects. In conclusion, present findings show that CoQ10 supplementation attenuated EE-induced cholestasis by promoting a favorable redox environment in the liver, and further suggest that it may represent an alternative therapeutic option for ICP.
Subject(s)
Cholestasis, Intrahepatic/drug therapy , Dietary Supplements , Pregnancy Complications/drug therapy , Ubiquinone/analogs & derivatives , Animals , Catalase/metabolism , Cholestasis, Intrahepatic/metabolism , Female , Glutathione/metabolism , Liver/drug effects , Liver/metabolism , Pregnancy , Pregnancy Complications/metabolism , Rats, Sprague-Dawley , Superoxide Dismutase/metabolism , Thiobarbituric Acid Reactive Substances/metabolism , Ubiquinone/pharmacology , Ubiquinone/therapeutic use , Ursodeoxycholic Acid/therapeutic useABSTRACT
INTRODUCTION: Primary stabbing headache (or "ice pick headache") is an alteration characterized by brief jabs (short stabs of pain, lasting ~3 seconds), which appear spontaneously, irregularly, and affecting unilaterally or bilaterally. Indomethacin has traditionally been used as the main therapeutic option. However, this drug is ineffective in a considerable percentage of patients and can generate multiple adverse effects that occur at therapeutic doses. CLINICAL CASE: A 7-year-old male patient with primary stabbing headache of mild to moderate intensity, lasting 3 to 4 seconds, without relevant history, with normal neurodevelopment, neurological examination and neuroimaging; no triggers were identified. It was started therapeutic trial with Coenzyme Q10; however, no improvement in the symptoms was identified. TREATMENT AND OUTCOMES: A therapeutic management was carried out with Melatonin, which led to complete remission of the symptoms; without adverse effects in the posterior follow-up months. CLINICAL AND SCIENTIFIC RELEVANCE: There is little information regarding effective and safe treatments for primary stabbing headache in children. The present case identifies Melatonin as an innovative, effective and safe therapeutic alternative in the treatment of primary stabbing headache in children. This is a significant advance in the understanding of primary stabbing headache in the pediatric population. CONCLUSION: Melatonin may be an effective and safe therapeutic option for the treatment of primary stabbing headache in pediatric patients. It is necessary to deepen its research, in order to establish its use in a clinical practice guide.
INTRODUCCIÓN: La cefalea punzante primaria, es una alteración que se caracteriza por punzadas breves (â¼3 segundos), que aparecen espontáneamente, de forma irregular y afectación unilateral o bilateral. Tradicionalmente se ha utilizado Indometacina como opción terapéutica principal. Sin embargo, este medicamento es inefectivo en un porcentaje considerable de pacientes y puede generar múltiples efectos adversos que se presentan a dosis terapéuticas. CASO CLÍNICO: Paciente masculino de 7 años de edad con cefalea punzante primaria de intensidad leve a moderada con una duración entre 3 y 4 segundos sin antecedentes relevantes, con neurodesarrollo, examen neurológico y de neuroimagen normales; no se identificaron desencadenantes. Se inició prueba terapéutica con Coenzima Q10, sin embargo no se identificó mejoría en los síntomas. TRATAMIENTO Y RESULTADOS: Se realizó un manejo terapéutico con Melatonina que conllevó a remisión completa de la sintomatología y sin efectos adversos en los meses posteriores de seguimiento. RELEVANCIA CLÍNICA Y CIENTÍFICA: Existe poca información respecto a tratamientos efectivos y seguros para cefalea punzante primaria en niños. El presente caso identifica la Melatonina como una alternativa terapéutica innovadora, efectiva y segura en el tratamiento de la cefalea punzante primaria en niños. Lo anterior constituye un avance significativo en la comprensión de la cefalea punzante primaria en la población pediátrica. CONCLUSIÓN: La melatonina puede ser una opción terapéutica efectiva y segura para el tratamiento de la cefalea punzante primaria en pacientes pediátricos. Se requiere ahondar en su investigación para establecer su uso en una guía de práctica clínica.
Subject(s)
Antioxidants/therapeutic use , Headache Disorders, Primary/prevention & control , Melatonin/therapeutic use , Antioxidants/adverse effects , Child , Follow-Up Studies , Headache Disorders, Primary/drug therapy , Humans , Male , Melatonin/adverse effects , Treatment Outcome , Ubiquinone/analogs & derivatives , Ubiquinone/therapeutic useABSTRACT
Mitochondrial dysfunction characterized by impaired bioenergetics, oxidative stress and aldehydic load is a hallmark of heart failure. Recently, different research groups have provided evidence that selective activation of mitochondrial detoxifying systems that counteract excessive accumulation of ROS, RNS and reactive aldehydes is sufficient to stop cardiac degeneration upon chronic stress, such as heart failure. Therefore, pharmacological and non-pharmacological approaches targeting mitochondria detoxification may play a critical role in the prevention or treatment of heart failure. In this review we discuss the most recent findings on the central role of mitochondrial dysfunction, oxidative stress and aldehydic load in heart failure, highlighting the most recent preclinical and clinical studies using mitochondria-targeted molecules and exercise training as effective tools against heart failure.
Subject(s)
Antioxidants/therapeutic use , Biomimetic Materials/therapeutic use , Cardiotonic Agents/therapeutic use , Heart Failure/therapy , Mitochondria, Heart/drug effects , Ubiquinone/analogs & derivatives , Aldehydes/antagonists & inhibitors , Aldehydes/metabolism , Animals , Clinical Trials as Topic , Disease Models, Animal , Drug Evaluation, Preclinical , Energy Metabolism/drug effects , Exercise , Heart Failure/metabolism , Heart Failure/pathology , Humans , Malondialdehyde/antagonists & inhibitors , Malondialdehyde/metabolism , Mitochondria, Heart/metabolism , Mitochondria, Heart/pathology , Oxidative Stress/drug effects , Reactive Nitrogen Species/antagonists & inhibitors , Reactive Nitrogen Species/metabolism , Reactive Oxygen Species/antagonists & inhibitors , Reactive Oxygen Species/metabolism , Superoxide Dismutase/chemistry , Ubiquinone/therapeutic useABSTRACT
Abstract Introduction: Primary stabbing headache (or "ice pick headache") is an alteration characterized by brief jabs (short stabs of pain, lasting ~3 seconds), which appear spontaneously, irregularly, and affecting unilaterally or bilaterally. Indomethacin has traditionally been used as the main therapeutic option. However, this drug is ineffective in a considerable percentage of patients and can generate multiple adverse effects that occur at therapeutic doses. Clinical case: A 7-year-old male patient with primary stabbing headache of mild to moderate intensity, lasting 3 to 4 seconds, without relevant history, with normal neurodevelopment, neurological examination and neuroimaging; no triggers were identified. It was started therapeutic trial with Coenzyme Q10; however, no improvement in the symptoms was identified. Treatment and outcomes: A therapeutic management was carried out with Melatonin, which led to complete remission of the symptoms; without adverse effects in the posterior follow-up months. Clinical and scientific relevance: There is little information regarding effective and safe treatments for primary stabbing headache in children. The present case identifies Melatonin as an innovative, effective and safe therapeutic alternative in the treatment of primary stabbing headache in children. This is a significant advance in the understanding of primary stabbing headache in the pediatric population. Conclusion: Melatonin may be an effective and safe therapeutic option for the treatment of primary stabbing headache in pediatric patients. It is necessary to deepen its research, in order to establish its use in a clinical practice guide.
Resumen Introducción: La cefalea punzante primaria, es una alteración que se caracteriza por punzadas breves (∼3 segundos), que aparecen espontáneamente, de forma irregular y afectación unilateral o bilateral. Tradicionalmente se ha utilizado Indometacina como opción terapéutica principal. Sin embargo, este medicamento es inefectivo en un porcentaje considerable de pacientes y puede generar múltiples efectos adversos que se presentan a dosis terapéuticas. Caso clínico: Paciente masculino de 7 años de edad con cefalea punzante primaria de intensidad leve a moderada con una duración entre 3 y 4 segundos sin antecedentes relevantes, con neurodesarrollo, examen neurológico y de neuroimagen normales; no se identificaron desencadenantes. Se inició prueba terapéutica con Coenzima Q10, sin embargo no se identificó mejoría en los síntomas. Tratamiento y resultados: Se realizó un manejo terapéutico con Melatonina que conllevó a remisión completa de la sintomatología y sin efectos adversos en los meses posteriores de seguimiento. Relevancia clínica y científica: Existe poca información respecto a tratamientos efectivos y seguros para cefalea punzante primaria en niños. El presente caso identifica la Melatonina como una alternativa terapéutica innovadora, efectiva y segura en el tratamiento de la cefalea punzante primaria en niños. Lo anterior constituye un avance significativo en la comprensión de la cefalea punzante primaria en la población pediátrica. Conclusión: La melatonina puede ser una opción terapéutica efectiva y segura para el tratamiento de la cefalea punzante primaria en pacientes pediátricos. Se requiere ahondar en su investigación para establecer su uso en una guía de práctica clínica.
Subject(s)
Child , Humans , Male , Headache Disorders, Primary/prevention & control , Melatonin/therapeutic use , Antioxidants/therapeutic use , Follow-Up Studies , Ubiquinone/analogs & derivatives , Ubiquinone/therapeutic use , Treatment Outcome , Headache Disorders, Primary/drug therapy , Melatonin/adverse effects , Antioxidants/adverse effectsABSTRACT
PURPOSE: Nitrogen mustard (NM) is a devastating casualty agent in chemical warfare. There is no effective antidote to treat NM-induced ocular injury. We aimed to assess the effects of proanthocyanidin (PAC) and coenzyme Q10 (CoQ10) on NM-induced ocular injury. METHODS: Eighteen male rats were divided into the following 4 groups: NM, NM + PAC, NM + CoQ10, and control. The 3 NM groups received a single dose of NM (0.02 mg/µL) on the right eye to induce ocular injury. The control group received saline only. Thirty minutes after the application of NM, the NM + PAC group received PAC (100 mg/kg) via gastric gavage, while the NM + CoQ10 group received CoQ10 (10 mg/kg) via intraperitoneal injection. PAC and CoQ10 were administered once a day for 5 consecutive days. The rats were then sacrificed. Macroscopic images of the eyes were examined and eye tissues were collected for histology. RESULTS: The treatment groups were compared to the control group with regard to both corneal opacity and lid injury scores. The findings were not significantly different for both the NM + PAC and NM + CoQ10 groups. In both the NM + PAC and NM + CoQ10 groups, the histological changes seen in the NM group demonstrated improvement. CONCLUSIONS: Our results indicate that PAC and CoQ10 treatments have therapeutic effects on NM-induced ocular injury in a rat model. PAC and CoQ10 may be novel options in patients with NM-induced ocular injury.
Subject(s)
Antioxidants/therapeutic use , Burns, Chemical/drug therapy , Eye Injuries/drug therapy , Proanthocyanidins/therapeutic use , Ubiquinone/analogs & derivatives , Animals , Chemical Warfare Agents , Disease Models, Animal , Eye Injuries/chemically induced , Male , Mechlorethamine , Random Allocation , Rats , Rats, Sprague-Dawley , Ubiquinone/therapeutic useABSTRACT
ABSTRACT Purpose: Nitrogen mustard (NM) is a devastating casualty agent in chemical warfare. There is no effective antidote to treat NM-induced ocular injury. We aimed to assess the effects of proanthocyanidin (PAC) and coenzyme Q10 (CoQ10) on NM-induced ocular injury. Methods: Eighteen male rats were divided into the following 4 groups: NM, NM + PAC, NM + CoQ10, and control. The 3 NM groups received a single dose of NM (0.02 mg/μL) on the right eye to induce ocular injury. The control group received saline only. Thirty minutes after the application of NM, the NM + PAC group received PAC (100 mg/kg) via gastric gavage, while the NM + CoQ10 group received CoQ10 (10 mg/kg) via intraperitoneal injection. PAC and CoQ10 were administered once a day for 5 consecutive days. The rats were then sacrificed. Macroscopic images of the eyes were examined and eye tissues were collected for histology. Results: The treatment groups were compared to the control group with regard to both corneal opacity and lid injury scores. The findings were not significantly different for both the NM + PAC and NM + CoQ10 groups. In both the NM + PAC and NM + CoQ10 groups, the histological changes seen in the NM group demonstrated improvement. Conclusions: Our results indicate that PAC and CoQ10 treatments have therapeutic effects on NM-induced ocular injury in a rat model. PAC and CoQ10 may be novel options in patients with NM-induced ocular injury.
RESUMO Objetivo: A mostarda de nitrogênio (MN) é um agente de guerra química devastador. Não existe um antídoto eficaz para tratar lesões oculares induzidas por MN. Nosso objetivo foi avaliar os efeitos da proantocianidina (PAC) e da coenzima Q10 (CoQ10) na lesão ocular induzida por MN. Métodos: Dezoito ratos machos foram divididos em 4 grupos: MN, MN + PAC, MN + CoQ10 e Controle. Três grupos receberam uma dose única de MN (0,02 mg/μL) destilada no olho direito para gerar lesão ocular. Os animais do grupo controle receberam apenas solução salina. Trinta minutos após a aplicação de MN nos animais, o grupo MN + PAC recebeu PAC (100 mg/kg) por gavagem gástrica, enquanto a CoQ10 (10 mg/kg) foi administrada ao grupo MN + CoQ10 por meio de injeção intraperitoneal. A administração de PAC e de CoQ10 foi realizada uma vez por dia, durante 5 dias consecutivos. Os ratos foram, então, sacrificados. Imagens macroscópicas dos olhos foram examinadas e tecidos oculares foram coletados para histologia. Resultados: Os grupos de tratamento foram comparados ao grupo de controle quanto à opacidade da córnea e quanto aos escores de lesão da cobertura da córnea. Os resultados foram insignificantes para ambos os grupos. Ambos, o grupo MN+PAC e o grupo MN+CoQ10, apresentaram melhoras das alterações histológicas observadas no grupo MN. Conclusões: Nossos resultados indicam que os tratamentos com PAC e com CoQ10 têm efeitos terapêuticos sobre lesões oculares induzidas por MN em um modelo em ratos. A proantocianidina e a CoQ10 podem ser uma nova opção nesses casos.
Subject(s)
Animals , Male , Rats , Burns, Chemical/drug therapy , Eye Injuries/drug therapy , Ubiquinone/analogs & derivatives , Proanthocyanidins/therapeutic use , Antioxidants/therapeutic use , Random Allocation , Chemical Warfare Agents , Eye Injuries/chemically induced , Ubiquinone/therapeutic use , Rats, Sprague-Dawley , Disease Models, Animal , MechlorethamineABSTRACT
OBJECTIVE: To assess the association between coenzyme Q10 (CoQ10) intake from food sources and semen quality. We assessed this association in a prospective cohort of men attending a fertility clinic. CoQ10 supplementation has been associated with improvements in semen parameters. However, the impact of CoQ10 intake from food sources on semen quality has not been investigated. MATERIALS AND METHODS: Subfertile couples seeking fertility evaluation at the Massachusetts General Hospital Fertility Center were invited to participate in an ongoing study of environmental factors and fertility. In total, 211 male participants completed a validated food frequency questionnaire and provided 476 semen samples. Multivariable linear mixed models were used to examine the relation between CoQ10 intake from food and semen parameters while adjusting for potential confounders and accounting for within-person correlations. RESULTS: Mean dietary CoQ10 intake was 19.2 mg/day (2.4-247.2 mg/day). No subjects were taking CoQ10 supplements. There were no associations between dietary CoQ10 intake from food and conventional semen parameters. The adjusted mean difference (95% confidence interval) comparing men in the top and bottom quartiles of CoQ10 intake from food were -3.1 mil/mL (95% confidence interval -29.5, 38.8 mil/mL) for sperm concentration, -4.5% (-15.1%, 6.0%) for total motility, -1.3% for progressive motility (-8.4%, 5.7%), and 0.3% (-1.4%, 2.0%) for sperm morphology. CONCLUSION: CoQ10 intake from food was not related to semen parameters among subfertile men. Mean dietary intake of CoQ10 in this study was 10-fold lower than the supplemental dose used in clinical trials showing improved sperm motility. CoQ10 intake from food alone may be insufficient to optimize semen parameters.
Subject(s)
Dietary Supplements , Food , Infertility, Male/diet therapy , Semen Analysis , Ubiquinone/analogs & derivatives , Vitamins/therapeutic use , Adult , Humans , Male , Prospective Studies , Ubiquinone/therapeutic useABSTRACT
PURPOSE: Corneal involvement in mitochondrial disease is seldom described. Kearns-Sayre syndrome (KSS) is a mitochondrial disorder characterized by retinitis pigmentosa, external ophthalmoplegia, and heart block. We report 2 patients with KSS with corneal lesions involving the endothelium, which improved with Coenzyme Q10 (CoQ10). Based on recent research regarding the role of dysfunctional oxidative metabolism in Fuchs Endothelial Corneal Dystrophy (FECD), we propose that mitochondrial diseases and FECD share a final pathway. METHODS: A chart review was performed and a review of the literature was completed with a PubMed search using the terms "Kearns-Sayre Syndrome", "mitochondria", "endothelium", "Fuchs endothelial corneal dystrophy", and "cornea". RESULTS: There are 19 reports of corneal involvement in clinical phenotypes of mitochondrial disease. Nine of these 19 cases had findings consistent with KSS. Our patients with KSS had microcystic changes throughout the cornea and excrescences on the endothelial surface seen with ultrasound biomicroscopy, similar to the clinical findings in FECD. CoQ10 improved corneal disease in both children. CoQ10 deficiency has been reported in a variety of mitochondrial diseases, and efficacy of supplementation has been demonstrated. It may be beneficial in these patients because of its antioxidant properties and role in oxidative phosphorylation. CONCLUSIONS: The common deletion found in patients with KSS has recently been implicated in FECD, which has recently been shown to be a disease related to dysfunctional oxidative metabolism. Future research should explore the use of antioxidants, such as CoQ10 in patients with FECD.
Subject(s)
Corneal Edema/drug therapy , Electron Transport Chain Complex Proteins/therapeutic use , Endothelium, Corneal/drug effects , Fuchs' Endothelial Dystrophy/drug therapy , Kearns-Sayre Syndrome/drug therapy , Ubiquinone/analogs & derivatives , Child , Child, Preschool , Corneal Edema/diagnosis , Endothelium, Corneal/pathology , Humans , Kearns-Sayre Syndrome/diagnosis , Male , Ophthalmic Solutions , Ubiquinone/therapeutic use , Visual Acuity/drug effectsABSTRACT
Mitochondrial diseases are a group of clinically heterogeneous disorders that can be difficult to diagnose. We report a two and a half year old girl with clinical symptoms compatible with Leigh disease but with no definitive diagnosis. Using next generation sequencing we found that mutation 3697G>A was responsible for the patient's clinical symptoms. Corroboration was performed via segregation analysis in mother and sister and by evolutionary analysis that showed that the mutation is located in a highly conserved region across a wide range of species. Functional analyses corroborated the mutation effect and indicated that the pathophysiological alterations were partially restored by Coenzyme Q10. In addition, we proposed that the presence of the mutation at high frequencies causes the phenotype in the patient, while other family members with intermediate levels of heteroplasmy are symptoms-free.
Subject(s)
Leigh Disease/genetics , NADH Dehydrogenase/genetics , Point Mutation , Child, Preschool , DNA, Mitochondrial/chemistry , DNA, Mitochondrial/genetics , Female , High-Throughput Nucleotide Sequencing , Humans , Ubiquinone/analogs & derivatives , Ubiquinone/therapeutic useABSTRACT
OBJECTIVE: Bipolar disorder places a significant burden on individuals, caregivers and family, and the broader community. Current treatments are believed to be more effective against manic symptoms, leaving a shortfall in recovery during the depressive phase of the illness. The current study draws on recent evidence suggesting that, in addition to increased oxidative load, alterations in mitochondrial function occur in bipolar disorder. METHODS: This 16-week study aims to explore the potential benefits of N-acetylcysteine (NAC) alone or in combination (CT) with selected nutraceuticals believed to enhance mitochondrial function. The study includes adults diagnosed with bipolar disorder currently experiencing an episode of depression. Participants are asked to take NAC, CT, or placebo in addition to any usual treatments. A post-discontinuation visit is conducted 4 weeks following the treatment phase. RESULTS: The primary outcome of the study will be mean change on the Montgomery-Asberg Depression Rating Scale. Secondary outcomes include functioning, substance use, mania ratings, and quality of life. Blood samples will be collected at baseline and week 16 to explore biochemical alterations following treatment. CONCLUSION: This study may provide a novel adjunctive treatment for bipolar depression. Analysis of biological samples may assist in understanding the therapeutic benefits and the underlying etiology of bipolar depression. TRIAL REGISTRATION: Australian and New Zealand Clinical Trial Registry ACTRN12612000830897.
Subject(s)
Acetylcysteine/therapeutic use , Bipolar Disorder/therapy , Depressive Disorder/therapy , Dietary Supplements , Free Radical Scavengers/therapeutic use , Mitochondrial Diseases/therapy , Adult , Antidepressive Agents/therapeutic use , Antioxidants/therapeutic use , Combined Modality Therapy/methods , Dose-Response Relationship, Drug , Double-Blind Method , Female , Humans , Male , Mitochondria/drug effects , Placebos/therapeutic use , Psychiatric Status Rating Scales , Statistics, Nonparametric , Time Factors , Treatment Outcome , Ubiquinone/analogs & derivatives , Ubiquinone/therapeutic use , Vitamin K 3/therapeutic use , Vitamins/therapeutic useSubject(s)
DNA, Mitochondrial/genetics , Micronutrients/therapeutic use , Mitochondrial Diseases/drug therapy , Mutation , Optic Atrophy, Hereditary, Leber/drug therapy , Ubiquinone/analogs & derivatives , Child , Humans , Male , Mitochondrial Diseases/genetics , Optic Atrophy, Hereditary, Leber/genetics , Pedigree , Polymerase Chain Reaction , Siblings , Treatment Outcome , Ubiquinone/therapeutic use , Visual Acuity/drug effects , Visual Fields/drug effectsABSTRACT
UNLABELLED: Recent studies have shown that the formation of myringosclerosis could be reduced by the application of antioxidant enzymes and elements. OBJECTIVE: The aim of this study was to investigate the effectiveness of coenzyme Q10 on the prevention of experimentally induced myringosclerosis. METHOD: Forty-eight healthy female wistar albino rats were bilaterally myringotomized and divided into four groups randomly. Group A received no treatment, group B was administered oral coenzyme Q10. Group C was treated with topical saline solution, group D received topically coenzyme Q10. On the 15th day of treatment, tympanic membranes were examined by otomicroscopy. Myringosclerotic lesions were documented semiquantitatively by using 4-point scale. After harvesting tympanic membranes were evaluated histopathologically. RESULTS: In group D (topical coenzyme Q10), we observed otitis within the first four days of the study and this group was excluded from the study. Regarding otomicroscopic examinations, there were no significant differences among groups in myringosclerosis formation (p = 0.241). When group A (non treatment) compared to groups B and C regarding histopathologic examination, the results demonstrated statistical significant differences (p = 0.004; p < 0.001), respectively. There was no statisticaly significant difference between groups B and C (p = 0.160). CONCLUSION: Oral administration of coenzyme Q10 did not reduce myringosclerosis formation in myringotomized rats.
Subject(s)
Myringosclerosis/prevention & control , Ubiquinone/analogs & derivatives , Vitamins/therapeutic use , Animals , Disease Models, Animal , Female , Myringoplasty , Myringosclerosis/pathology , Random Allocation , Rats , Rats, Wistar , Ubiquinone/therapeutic useABSTRACT
Estudos recentes demonstram que a formação de miringoesclerose pode ser reduzida pela aplicação de enzimas e elementos antioxidantes. OBJETIVO: Investigar a eficácia da coenzima Q10 na prevenção de miringoesclerose experimentalmente induzida. MÉTODO: Quarenta e oito ratas Wistar albinas saudáveis sofreram miringotomia e foram divididas aleatoriamente em quatro grupos. O Grupo A não recebeu tratamento algum; o Grupo B recebeu coenzima Q10 por via oral; o Grupo C foi tratado com soro fisiológico tópico; e o Grupo D recebeu coenzima Q10 tópica. No 15º dia de tratamento, as membranas timpânicas foram examinadas por otomicroscopia. As lesões miringoescleróticas foram documentadas de forma semiquantitativa por meio de uma escala de quatro pontos. Após a coleta, as membranas timpânicas foram avaliadas por histopatologia. RESULTADOS: No grupo D (coenzima Q10 tópica) foi observada a ocorrência de otite nos primeiros quatro dias do estudo, o que levou à sua exclusão do estudo. O exame de otomicroscopia não revelou diferenças significativas entre grupos em termos de formação de miringoesclerose (p = 0,241). Diferenças estatisticamente significativas foram observada quando os exames histopatológicos do grupo A foram comparados aos dos grupos B e C (p = 0,004; p < 0,001, respectivamente). Não houve diferença significativa entre os grupos B e C (p = 0,160). CONCLUSÃO: A administração oral de coenzima Q10 não reduziu a formação de miringoesclerose nos ratos submetidos à miringotomia.
Recent studies have shown that the formation of myringosclerosis could be reduced by the application of antioxidant enzymes and elements. OBJECTIVE: The aim of this study was to investigate the effectiveness of coenzyme Q10 on the prevention of experimentally induced myringosclerosis. METHOD: Forty-eight healthy female wistar albino rats were bilaterally myringotomized and divided into four groups randomly. Group A received no treatment, group B was administered oral coenzyme Q10. Group C was treated with topical saline solution, group D received topically coenzyme Q10. On the 15th day of treatment, tympanic membranes were examined by otomicroscopy. Myringosclerotic lesions were documented semiquantitatively by using 4-point scale. After harvesting tympanic membranes were evaluated histopathologically. RESULTS: In group D (topical coenzyme Q10), we observed otitis within the first four days of the study and this group was excluded from the study. Regarding otomicroscopic examinations, there were no significant differences among groups in myringosclerosis formation (p = 0.241). When group A (non treatment) compared to groups B and C regarding histopathologic examination, the results demonstrated statistical significant differences (p = 0.004; p < 0.001), respectively. There was no statisticaly significant difference between groups B and C (p = 0.160). CONCLUSION: Oral administration of coenzyme Q10 did not reduce myringosclerosis formation in myringotomized rats.
Subject(s)
Animals , Female , Rats , Myringosclerosis/prevention & control , Ubiquinone/analogs & derivatives , Vitamins/therapeutic use , Disease Models, Animal , Myringoplasty , Myringosclerosis/pathology , Random Allocation , Rats, Wistar , Ubiquinone/therapeutic useABSTRACT
Dysferlinopathy is a form of muscular dystrophy affecting muscles of the shoulder and pelvic girdles, resulting from inheritance of a mutated dysferlin gene. The encoded dysferlin protein is proposed to be involved in sarcolemmal vesicle fusion with a disrupted plasma membrane; however, with defective protein function these vesicles accumulate beneath the disruption site but are unable to fuse with it and reseal the membrane, thus rendering the membrane repair mechanism defective. The SJL/J mouse model presents with characteristics much like the commonest human condition. Immune modulators have long been under study in the maintenance of muscle health in muscular dystrophies. Such supplementary treatment would ideally suppress inflammation, preventing the immune response toward degenerating muscle from causing additional muscle fiber death, and thus provide a mechanism by which to prolong the life of muscle fibers with inherently defective healing apparatus. For this purpose the anti-inflammatory supplement resveratrol and the membrane-protective supplement coenzyme Q10 were administered separately and in combination to experimental animals to determine their effectiveness in possible therapy of dysferlinopathy. The findings of this study report that low doses of resveratrol and coenzyme Q10 supplementation in exclusivity were unable to afford much protection to muscle fibers at the tissue level. High doses of coenzyme Q10 proved more effective in reducing attenuating inflammation; and combination treatment with resveratrol and coenzyme Q10 provided not only the membrane-protective effects of coenzyme Q10, but also the anti-inflammatory effects of resveratrol which failed to materialize at sufficient levels in exclusive administration.
Disferlinopatía es una forma de distrofia muscular que afecta a los músculos de los hombros y cintura pélvica, resultado de la herencia y mutación del gen de la distrofina. Sugerimos que la proteína codificada distrofina que integra la estructura sarcolemal con una membrana plasmática interrumpida, que al presentar una proteína defectuosa, las estructuras se acumulan debajo del sitio de alteración sin lograr fundirse con éste y cerrar la membrana afectando el mecanismo de reparación. El modelo de ratón SJL / J se presenta con características muy similares a una condición humana común. Los inmunomoduladores han sido objeto de estudio en el mantenimiento de la salud muscular en las distrofias musculares. Este tipo de tratamiento suplementario puede ser ideal para suprimir la inflamación, en la prevención de la respuesta inmune en la degeneración muscular causando la muerte adicional de fibra muscular, y al mismo tiempo proporcionar, un mecanismo con el cual prolongar la vida útil de aquellas fibras musculares con el aparato de sanación comprometido. Para ello, el Resveratrol suplemento anti-inflamatorio y el suplemento protector de membrana coenzima Q10 se administró por separado y en combinación en los animales de laboratorio para determinar su efectividad en el tratamiento de posible disferlinopatía. Los resultados de este estudio indican que el Resveratrol en menor dosis y la coenzima Q 10 administrados como suplementos de manera exclusiva, no demostraron efectos de protección de las fibras musculares a nivel del tejido. Una alta dosis de coenzima Q10 demostró ser más efectiva en la reducción de la inflamación; adicionalmente, el tratamiento combinado de Resveratrol y coenzima Q10 proporcionó efectos protectores de membrana, además de los efectos anti-inflamatorios del Resveratrol cuyo nivel no alcanzó la efectividad suficiente al ser administrado en forma exclusiva.
Subject(s)
Rats , Muscular Dystrophies, Limb-Girdle/drug therapy , Muscular Dystrophies, Limb-Girdle/therapy , Sarcolemma , Sarcolemma/immunology , Stilbenes/administration & dosage , Stilbenes/therapeutic use , Rats/growth & development , Rats/injuries , Ubiquinone/immunology , Ubiquinone/therapeutic useABSTRACT
OBJECTIVE: To assess whether supplementation with Coenzyme Q10 (CoQ10) during pregnancy reduces the risk of pre-eclampsia. METHODS: Women at increased risk of pre-eclampsia were enrolled in a randomized, double-blind, placebo-controlled trial. Women were assigned to receive 200 mg of CoQ10 or placebo daily from 20 weeks of pregnancy until delivery. The primary outcome was rate of pre-eclampsia. Statistical analyses were by intention-to-treat. RESULTS: Of the 235 women enrolled in the trial, 118 were randomized to receive CoQ10 and 117 received a placebo. A total of 197 (83.8%) women were followed-up. The overall rate of pre-eclampsia was 20% (n=47). Thirty women (25.6%) in the placebo group developed pre-eclampsia compared with 17 women (14.4%) in the CoQ10 group, and this reduction was significant (P=0.035) (relative risk [RR] 0.56; 95% confidence interval [CI], 0.33-0.96). CONCLUSION: Supplementation with CoQ10 reduces the risk of developing pre-eclampsia in women at risk for the condition.
Subject(s)
Pre-Eclampsia/prevention & control , Ubiquinone/analogs & derivatives , Vitamins/therapeutic use , Adolescent , Data Interpretation, Statistical , Double-Blind Method , Female , Follow-Up Studies , Humans , Pregnancy , Risk Factors , Ubiquinone/therapeutic use , Young AdultABSTRACT
Nuestra piel está constantemente expuesta al estrés oxidativo endógeno y exógeno, el cual juega un papel fundamental tanto en el envejecimiento intrínseco como extrínseco. El estrés oxidativo se debe a la producción de especies reactivas de oxígeno, también conocidas como radicales libres. Las estructuras vitales que se ven afectadas por este proceso son el ADN, elementos del citoesqueleto, proteínas celulares y membranas celulares. El cuerpo posee mecanismos de defensa contra los radicales libres, denominados antioxidantes, los cuales son capaces de reducirlos y neutralizarlos. Sin embargo, como parte natural del proceso de envejecimiento, no sólo la producción de especies reactivas de oxígeno aumenta, sino que los mecanismos endógenos de defensa disminuyen, resultando en un desbalance con predominio de radicales libres no neutralizados que dañan las estructuras del organismo. Aunque el cuerpo posee antioxidantes endógenos y ciertos alimentos son ricos en antioxidantes, muchos creen que niveles más altos de estas sustancias pueden obtenerse con suplementos alimentarios. En consecuencia, ha llegado a ser muy popular el uso de antioxidantes en suplementos orales o en forma tópica, los cuales podrían potencialmente aminorar los efectos adversos de las especies reactivas de oxígeno. En esta revisión se analizan los antioxidantes más conocidos que se encuentran incorporados en los productos cosméticos o que son administrados por vía oral en los pacientes interesados en la cosmética personal.
Our skin is constantly exposed to endogenous and exogenous oxidative stress, which plays a pivotal role in intrinsic and extrinsic aging. Oxidative stress is delivered by the creation of reactive oxygen species also known as free radicals. Vital structures that can be adversely affected by this process are DNA, cytoskeletal elements, cellular proteins, and cellular membranes. The body possesses defense mechanisms against free radicals, which are called antioxidants, and are able to reduce and neutralize them. However, as part of the natural aging process, not only does the production of reactive oxygen species increase, but our endogenous defense mechanisms decrease resulting in an imbalance and increased number of unchecked free radicals damaging vital structures of the body. Although the body possesses endogenous antioxidants and certain foods are rich in antioxidants, many believe that higher levels can be achieved by supplementation. Consequently, the use of antioxidants as oral supplements or topical formulation should be able to lessen the harmful adverse effects induced by reactive oxygen species and has thus become popular. This review discusses the most popular types of antioxidants found in cosmetic products or taken orally by cosmetic patients.
Subject(s)
Humans , Antioxidants/therapeutic use , Skin Aging , Ascorbic Acid/therapeutic use , Coffee/chemistry , Carotenoids/therapeutic use , Curcumin/therapeutic use , Stilbenes/therapeutic use , Plant Extracts/therapeutic use , Polypodium/chemistry , Silymarin/therapeutic use , Tea , Ubiquinone/analogs & derivatives , Ubiquinone/therapeutic use , Vitamin E/therapeutic useABSTRACT
Maternally inherited diabetes and deafness (MIDD) has been related to an A to G transition in the mitochondrial tRNA Leu (UUR) gene at the base pair 3243. This subtype of diabetes is characterized by maternal transmission, young age at onset and bilateral hearing impairment. Besides diabetes and deafness, the main diagnostic features, a wide range of multisystemic symptoms may be associated with the A3243G mutation. Organs that are most metabolically active, such as muscles, myocardium, retina, cochlea, kidney and brain are frequently affected. Gastrointestinal tract symptoms are also common in patients with mitochondrial disease and constipation and diarrhea are the most frequent manifestations. However, there are few prior reports of intestinal pseudo obstruction in MIDD patients. Here we report the case of a patient with MIDD associated with the mtDNA A3243G mutation who developed chronic intestinal pseudo obstruction, and the introduction of Coenzyme Q10 as adjunctive therapy led to a solution of the pseudo obstruction.
Diabetes mitocondrial ou diabetes e surdez de herança maternal (MIDD, acrônimo de maternally inherited diabetes and deafness) é freqüentemente associado à mutação mitocondrial A3243G. Esse subtipo de diabetes é caracterizado por transmissão materna, disacusia neuro-sensorial bilateral e idade precoce de aparecimento. Além do diabetes e da surdez, principais características diagnósticas, outros sintomas em diferentes órgãos podem também associar-se à mutação A3243G. Os órgãos que são metabolicamente mais ativos, tais como músculos, miocárdio, retina, cóclea, rim e cérebro, são freqüentemente afetados. Sintomas do trato gastrintestinal também são comuns em pacientes com doença mitocondrial, sendo diarréia e obstipação as manifestações mais freqüentes. Entretanto, há poucos relatos de pseudo-obstrução intestinal em portadores de diabetes mitocondrial. Este relato descreve o caso de uma paciente com diabetes mitocondrial que apresentou pseudo-obstrução intestinal e que com a introdução de coenzima Q10, como terapia adjunta, teve resolução o quadro.