Coenzyme Q10 and its effects in the treatment of neurodegenerative diseases

According to clinical and pre-clinical studies, oxidative stress and its consequences may be the cause or, at least, a contributing factor, to a large number of neurodegenerative diseases. These diseases include common and debilitating disorders, characterized by progressive and irreversible loss of neurons in specific regions of the brain. The most common neurodegenerative diseases are Parkinson's disease, Huntington's disease, Alzheimer's disease and amyotrophic lateral sclerosis. Coenzyme Q10 (CoQ10) has been extensively studied since its discovery in 1957. It is a component of the electron transportation chain and participates in aerobic cellular respiration, generating energy in the form of adenosine triphosphate (ATP). The property of CoQ10 to act as an antioxidant or a pro-oxidant, suggests that it also plays an important role in the modulation of redox cellular status under physiological and pathological conditions, also performing a role in the ageing process. In several animal models of neurodegenerative diseases, CoQ10 has shown beneficial effects in reducing disease progression. However, further studies are needed to assess the outcome and effectiveness of CoQ10 before exposing patients to unnecessary health risks at significant costs.De acordo com estudos clínicos e pré-clínicos, o estresse oxidativo e suas conseqüências podem ser a causa, ou, no mínimo, o fator que contribui para grande número de doenças degenerativas. Estas doenças incluem problemas comuns e debilitantes, caracterizados por perda progressiva e irreversível de neurônios em regiões específicas do cérebro. As doenças degenerativas mais comuns são doença de Parkinson, de Hutington, de Alzheimer e esclerose amiotrófica lateral. A Coenzima Q10 (CoQ10) tem sido intensamente estudada desde sua descoberta, em 1957. É um componente da cadeia de transporte eletrônico e participa da respiração aeróbica celular, gerando energia na forma de trifosfato de adenosina (ATP). A propriedade da CoQ10 de atuar como antioxidante ou pró-oxidante sugere papel importante na modulação do estado redox celular sob condições fisiológicas e patológicas, desempenhando, também, papel no processo de envelhecimento. Em vários modelos animais de doenças neurodegenerativas, a CoQ10 mostrou efeitos benéficos na redução do curso da doença. Entretanto, há necessidade de estudos adicionais para avaliar o efeito e a eficácia da CoQ10 antes de expor os pacientes a riscos de saúde desnecessários e de alto custo

Continuous Catalyst-Free Esterification of Oleic Acid in Compressed Ethanol

The esterification of oleic acid in a continuous catalyst-free process using compressed ethanol was investigated in the present study. Experiments were performed in a tubular reactor and variables investigated were temperature, pressure, and oleic acid to ethanol molar ratio for different residence time. Results demonstrated that temperature, in the range of 473 K to 573 K, and pressure had a positive effect on fatty acid ethyl esters (FAEE) production. In the experimental range investigated, high conversions can be obtained at low ethanol concentrations in the reaction medium and it was observed that oleic acid to ethanol molar ratios greater than 1 : 6 show no significant increase in conversion. Nonnegligible reaction conversions (>90%) were achieved at 573 K, 20 MPa, oleic acid to ethanol molar ratio of 1 : 6, and 20 minutes of residence time

Motivação ao seguimento terapêutico das doenças cardiovasculares: revisão integrativa

Introduction: Cardiovascular diseases are a major concern for global health. The lack of therapeutic follow-up for these diseases is associated with a high risk of cardiovascular events. Understanding the elements that motivate this adherence can prompt the development of more effective interventions. Objective: To identify the regulatory elements that regulate the motivation for the therapeutic follow-up of cardiovascular diseases. Methods: This is an integrative review following Whitemore and Knafl's guidelines. The articles were selected between December 2020 and January 2021 in the databases: LILACS, SciELO, MEDLINE and Cochrane Library, with a time frame from 2011 to 2021, in Portuguese, English and Spanish. Review articles, reflections, guidelines, research protocols, and repeated articles were excluded. 19 articles were selected. Results: Studies from 12 countries showed the regulators of motivation for the treatment of cardiovascular diseases in five categories: social support, physical health, self-determination, psycho-emotional regulators and care systems. Conclusion: In essence, motivation has complex regulations that mobilize and enhance human behavior. The results can guide nursing care and intentional actions that influence the therapeutic follow-up of cardiovascular diseases, improving health outcomes.Introducción: Las enfermedades cardiovasculares son una preocupación importante para la salud mundial. La falta de seguimiento terapéutico de estas enfermedades se asocia con un alto riesgo de eventos cardiovasculares. Comprender los elementos que motivan esta adherencia puede impulsar el desarrollo de intervenciones más efectivas. Objetivo: Identificar los elementos reguladores de la motivación para el seguimiento terapéutico de las enfermedades cardiovasculares. Métodos: Se trata de una revisión integradora, siguiendo los lineamientos de Whitemore y Knafl. La selección de artículos se realizó entre diciembre de 2020 y enero de 2021 en las bases de datos LILACS, SciELO, MEDLINE y Cochrane Library. El marco temporal establecido para la selección fue de 2011 a 2021 y los idiomas fueron portugués, inglés y español. Se excluyeron artículos de revisión, reflexiones, guías, protocolos de investigación y artículos repetidos. Se seleccionaron 19 artículos. Resultados: Estudios de 12 países mostraron los reguladores de la motivación para el tratamiento de enfermedades cardiovasculares en cinco categorías: apoyo social, salud física, autodeterminación, reguladores psicoemocionales y sistemas de atención. Conclusión: En esencia, la motivación tiene regulaciones complejas que movilizan y mejoran el comportamiento humano. Los resultados pueden orientar los cuidados de enfermería y las acciones intencionales que influyen en el seguimiento terapéutico de las enfermedades cardiovasculares, mejorando los resultados de salud.Introdução: As doenças cardiovasculares são uma grande preocupação para a saúde mundial. A falta de seguimento terapêutico dessas doenças está associada com o alto risco de eventos cardiovasculares. Compreender os elementos que motivam essa adesão pode impulsionar a elaboração de intervenções mais efetivas. Objetivo: Identificar os elementos reguladores da motivação ao seguimento terapêutico das doenças cardiovasculares. Metodologia: Trata-se de uma revisão integrativa segundo as diretrizes de Whitemore e Knafl. Realizou-se a seleção dos artigos entre dezembro de 2020 e janeiro de 2021 nas bases de dados: LILACS, SciELO, MEDLINE e Cochrane Library, com recorte temporal de 2011 a 2021, nos idiomas português, inglês e espanhol. Foram excluídos os artigos de revisão, reflexão, guidelines, protocolos de pesquisa e artigos repetidos. 19 estudos foram selecionados. Resultados: Estudos oriundos de 12 países, mostraram os reguladores de motivação ao tratamento das doenças cardiovasculares em cinco categorias: suporte social, saúde física, autodeterminação, reguladores psicoemocionais e sistemas de cuidado. Conclusão: A motivação apresenta regulações complexas, que mobilizam e potencializam o comportamento humano. Os resultados podem direcionar a assistência de enfermagem e as ações intencionais que influenciem no seguimento terapêutico de doenças cardiovasculares, melhorando os resultados de saúde

Chronic renal effects in workers exposed to lead and their relationship with blood pressure

Neste estudo, foram determinadas as atividades de duas enzimas de membrana: alanina-aminopeptidase (AAP) e Y-glutamil-transpeptidase (YGT) e da enzima lisossomal N-acetil-B-D-glucosaminidase (NAG), bem como os níveis de proteína total (PT), albumina (ALB) e ácido delta-aminolevulínico (ALA) em urinas de indivíduos expostos ocupacionalmente ao chumbo (grupo exposto) e de indivíduos não expostos ao chumbo e nem a outras substâncias químicas (grupo controle). Todos os indivíduos apresentavam creatinina sérica inferior a 1,5 mg/dL. Ao mesmo tempo foram determinados os níveis sangfiíneos de chumbo (Pb-S) e aferidas pressão arterial diastólica (PD) e pressa-o arterial sistólica (PS). O objetivo foi investigar a toxicidade renal crônica do chumbo e sua possível correlação com a pressão arterial em indivíduos com função renal normal. A mediana de chumbo no sangue no grupo controle foi de 11,5 pg/dL contra 36,8 pg/dL no grupo exposto, mostrando-se dependente do tempo de exposição (p < 0,001). O valor mediano da NAG-U corrigido pela creatinina foi mais alto no grupo exposto (31,74 U/g creatinina) e significativamente diferente do grupo controle (25,28 U/g creatinina), p < 0,001. A atividade NAG-U se correlacionou com o Pb-S (p < 0,001), tempo de exposição (p < 0,001) e ALA-U (p < 0,001), mas não houve correlação com a pressão arterial. Os demais indicadores de função renal, Y GT-U, AAP-U, PT-U e ALB-U não se mostraram mais elevados no grupo controle e nem mostraram correlação com o Pb-S, tempo de exposição ou pressão arterial. A pressão arterial diastólica foi maior no grupo exposto (83 mmHg contra 78 mmHg no grupo controle) mas não se observaram diferenças quanto à pressão sistólica. Observaram-se correlações das pressoes arteriais diastólica e sistólica com tempo de exposição (p < 0,001 e p < 0,05 ) e com chumbo no sangue (p < 0,05 e p < 0,05 ) respectivamente, enquanto somente a pressão diastólica se correlacionou com o ALA-U (p < 0,05).In the present study we determined the activity of two renal tubule membrane enzymes: alanine-aminopeptidase (AAP) and Y-glutamyl-transpeptidase (YGT), and of the renal tubule lysosomal enzyme N-acetyl-B-D-glucosaminidase (NAG), as well as the levels of total protein (TP), albumin (ALB) and delta-aminolevulinic acid (ALA) in the urine of individuais occupationally exposed to lead (exposed group) and in individuais not exposed to lead or to any other chemical substances (control group). All individuais presented serum creatinine levels of less than 1.5 mg%. All subjects were also submitted to measurement of blood lead levels (B-Pb) and of diastolic and systolic arterial pressure. The objective was to investigate the chronic renal toxicity of lead and its possible correlation with arterial pressure in individuais with normal renal function. Median B-Pb levels were 11.5 pg/dL for the controls versus 36.8 Pg/dL for the exposed group, with the level being proportional to time o f exposure (p < 0.001). Median NAG-U values corrected for creatinine were higher in the exposed group (31.74 U/g creatinine) and significantly different from the control (25.28 U/g creatinine), p < 0.001. NAG-U activity was correlated with B-Pb (p < 0.001), time of exposure (p < 0.001) and ALA-U (p < O. 001), but not with arterial pressure. The remaining indicators of renal function, YGT-U, AAP-U, TP-U and ALB-U were not more elevated in the control group and were not correlated with B-Pb, time of exposure or arterial pressure. Diastolic arterial pressure was higher in the exposed group (83 mmHg versus 78 mmHg for the controls), but the two groups did not differ in systolic pressure. Diastolic and systolic pressure values were correlated with time of exposure (p < 0.001 and p < 0.05) and blood lead (p < 0,05 e 0,05) respectively but only diastolic pressure was correlated with ALA-U ( p < 0.05)

Chronic renal effects in workers exposed to lead and their relationship with blood pressure

Neste estudo, foram determinadas as atividades de duas enzimas de membrana: alanina-aminopeptidase (AAP) e Y-glutamil-transpeptidase (YGT) e da enzima lisossomal N-acetil-B-D-glucosaminidase (NAG), bem como os níveis de proteína total (PT), albumina (ALB) e ácido delta-aminolevulínico (ALA) em urinas de indivíduos expostos ocupacionalmente ao chumbo (grupo exposto) e de indivíduos não expostos ao chumbo e nem a outras substâncias químicas (grupo controle). Todos os indivíduos apresentavam creatinina sérica inferior a 1,5 mg/dL. Ao mesmo tempo foram determinados os níveis sangfiíneos de chumbo (Pb-S) e aferidas pressão arterial diastólica (PD) e pressa-o arterial sistólica (PS). O objetivo foi investigar a toxicidade renal crônica do chumbo e sua possível correlação com a pressão arterial em indivíduos com função renal normal. A mediana de chumbo no sangue no grupo controle foi de 11,5 pg/dL contra 36,8 pg/dL no grupo exposto, mostrando-se dependente do tempo de exposição (p < 0,001). O valor mediano da NAG-U corrigido pela creatinina foi mais alto no grupo exposto (31,74 U/g creatinina) e significativamente diferente do grupo controle (25,28 U/g creatinina), p < 0,001. A atividade NAG-U se correlacionou com o Pb-S (p < 0,001), tempo de exposição (p < 0,001) e ALA-U (p < 0,001), mas não houve correlação com a pressão arterial. Os demais indicadores de função renal, Y GT-U, AAP-U, PT-U e ALB-U não se mostraram mais elevados no grupo controle e nem mostraram correlação com o Pb-S, tempo de exposição ou pressão arterial. A pressão arterial diastólica foi maior no grupo exposto (83 mmHg contra 78 mmHg no grupo controle) mas não se observaram diferenças quanto à pressão sistólica. Observaram-se correlações das pressoes arteriais diastólica e sistólica com tempo de exposição (p < 0,001 e p < 0,05 ) e com chumbo no sangue (p < 0,05 e p < 0,05 ) respectivamente, enquanto somente a pressão diastólica se correlacionou com o ALA-U (p < 0,05).In the present study we determined the activity of two renal tubule membrane enzymes: alanine-aminopeptidase (AAP) and Y-glutamyl-transpeptidase (YGT), and of the renal tubule lysosomal enzyme N-acetyl-B-D-glucosaminidase (NAG), as well as the levels of total protein (TP), albumin (ALB) and delta-aminolevulinic acid (ALA) in the urine of individuais occupationally exposed to lead (exposed group) and in individuais not exposed to lead or to any other chemical substances (control group). All individuais presented serum creatinine levels of less than 1.5 mg%. All subjects were also submitted to measurement of blood lead levels (B-Pb) and of diastolic and systolic arterial pressure. The objective was to investigate the chronic renal toxicity of lead and its possible correlation with arterial pressure in individuais with normal renal function. Median B-Pb levels were 11.5 pg/dL for the controls versus 36.8 Pg/dL for the exposed group, with the level being proportional to time o f exposure (p < 0.001). Median NAG-U values corrected for creatinine were higher in the exposed group (31.74 U/g creatinine) and significantly different from the control (25.28 U/g creatinine), p < 0.001. NAG-U activity was correlated with B-Pb (p < 0.001), time of exposure (p < 0.001) and ALA-U (p < O. 001), but not with arterial pressure. The remaining indicators of renal function, YGT-U, AAP-U, TP-U and ALB-U were not more elevated in the control group and were not correlated with B-Pb, time of exposure or arterial pressure. Diastolic arterial pressure was higher in the exposed group (83 mmHg versus 78 mmHg for the controls), but the two groups did not differ in systolic pressure. Diastolic and systolic pressure values were correlated with time of exposure (p < 0.001 and p < 0.05) and blood lead (p < 0,05 e 0,05) respectively but only diastolic pressure was correlated with ALA-U ( p < 0.05)

Coenzyme Q10 and its effects in the treatment of neurodegenerative diseases

According to clinical and pre-clinical studies, oxidative stress and its consequences may be the cause or, at least, a contributing factor, to a large number of neurodegenerative diseases. These diseases include common and debilitating disorders, characterized by progressive and irreversible loss of neurons in specific regions of the brain. The most common neurodegenerative diseases are Parkinson's disease, Huntington's disease, Alzheimer's disease and amyotrophic lateral sclerosis. Coenzyme Q10 (CoQ10) has been extensively studied since its discovery in 1957. It is a component of the electron transportation chain and participates in aerobic cellular respiration, generating energy in the form of adenosine triphosphate (ATP). The property of CoQ10 to act as an antioxidant or a pro-oxidant, suggests that it also plays an important role in the modulation of redox cellular status under physiological and pathological conditions, also performing a role in the ageing process. In several animal models of neurodegenerative diseases, CoQ10 has shown beneficial effects in reducing disease progression. However, further studies are needed to assess the outcome and effectiveness of CoQ10 before exposing patients to unnecessary health risks at significant costs.<br>De acordo com estudos clínicos e pré-clínicos, o estresse oxidativo e suas conseqüências podem ser a causa, ou, no mínimo, o fator que contribui para grande número de doenças degenerativas. Estas doenças incluem problemas comuns e debilitantes, caracterizados por perda progressiva e irreversível de neurônios em regiões específicas do cérebro. As doenças degenerativas mais comuns são doença de Parkinson, de Hutington, de Alzheimer e esclerose amiotrófica lateral. A Coenzima Q10 (CoQ10) tem sido intensamente estudada desde sua descoberta, em 1957. É um componente da cadeia de transporte eletrônico e participa da respiração aeróbica celular, gerando energia na forma de trifosfato de adenosina (ATP). A propriedade da CoQ10 de atuar como antioxidante ou pró-oxidante sugere papel importante na modulação do estado redox celular sob condições fisiológicas e patológicas, desempenhando, também, papel no processo de envelhecimento. Em vários modelos animais de doenças neurodegenerativas, a CoQ10 mostrou efeitos benéficos na redução do curso da doença. Entretanto, há necessidade de estudos adicionais para avaliar o efeito e a eficácia da CoQ10 antes de expor os pacientes a riscos de saúde desnecessários e de alto custo

Carvedilol efficiently protects kidneys without affecting the antitumor efficacy of cisplatin in mice

Cisplatin is an effective anticancer drug which has been used to treat a wide range of tumors for the last 30 years. However, its use is associated with nephrotoxicity. Protective strategies have been reported, but their impact on the antitumor activity of cisplatin has not been clarified. We have previously reported the protective potential of carvedilol against cisplatin nephrotoxicity in tumor-free rats. Therefore, in the present study we used a tumor-bearing model to investigate the impact of carvedilol on the antitumor activity of cisplatin. The renal damage induced by cisplatin and the protective effect of carvedilol were demonstrated by the levels of blood urea nitrogen and plasma creatinine as well as by renal histopathology and immunohistochemistry. The mechanism of protection was associated with significantly decreased (i) oxidative stress markers, (ii) Bax expression, (iii) caspase-3 activity and (iv) TUNEL labeling for apoptosis. More importantly, evaluation of tumor mass, tumor remission rate and the survival curve showed that carvedilol did not impair the antitumor action of cisplatin. These findings suggest that the mechanisms underlying the nephrotoxic and the antitumor activity of cisplatin might be different. This is the first study to report such findings. Compared to other reported potential cytoprotectors against cisplatin-induced nephrotoxicity, carvedilol stands out due to the fact that it is already clinically-employed and well tolerated by the patients. Based on these features and on the present findings, carvedilol is a very promising candidate for future clinical trials as nephroprotector in patients treated with cisplatin

Protective effect of bixin on cisplatin-induced genotoxicity in PC12 cells

Bixin is the main carotenoid found in annatto seeds (Bixa orellana L.) and is responsible for their reddish-orange color. The antioxidant properties of this compound are associated with its ability to scavenge free radicals, which may reduce damage and protect tissues against toxicity caused by anticancer drugs such as cisplatin. In this study, the genotoxicity and antigenotoxicity of bixin on cisplatin-induced toxicity in PC12 cells was assessed. Cytotoxicity was evaluated using the mu assay, mutagenicity, genotoxicity, and protective effect of bixin were evaluated using the micronucleus test and comet assay. PC12 cells were treated with bixin (0.05, 0.08, and 0.10 mu g/mL), cisplatin (0.1 mu g/mL) or a combination of both bixin and cisplatin. Bixin was neither cytotoxic nor genotoxic compared to the controls. In the combined treatment bixin significantly reduced the percentage of DNA in tail and the frequency of micronuclei induced by cisplatin. This result suggests that bixin can function as a protective agent, reducing cisplatin-induced DNA damage in PC12 cells, and it is possible that this protection could also extend to neuronal cells. Further studies are being conducted to better understand the mechanisms involved in the activity of this protective agent prior to using it therapeutically. (C) 2011 Elsevier Ltd. All rights reserved.CNPq [470214/2008-2]CNP

Carvedilol protects the kidneys of tumor-bearing mice without impairing the biodistribution or the genotoxicity of cisplatin

Cisplatin (Cisp) is an effective antitumor drug; however, it causes severe nephrotoxicity. Minimization of renal toxicity is essential, but the interference of nephroprotective agents, particularly antioxidants, with the antitumor activity of cisplatin is a general concern. We have recently demonstrated that the anti-hypertensive and antioxidant drug carvedilol (CV) protects against the renal damage and increases the survival of tumor–bearing mice without impairing the tumor reduction by cisplatin. So far, reports on the antioxidant mechanism of CV are controversial and there are no data on the impact of CV on the antitumor mechanisms of cisplatin. Therefore, this study addresses the effect of CV on mechanisms underlying the tumor control by cisplatin. CV did not interfere with the biodistribution or the genotoxicity of cisplatin. We also addressed the antioxidant mechanisms of CV and demonstrated that it does not neutralize free radicals, but is an efficient chelator of ferrous ions that are relevant catalyzers in cisplatin nephrotoxicity. The present data suggest that oxidative damage and genotoxicity play different roles in the toxicity of cisplatin on kidneys and tumors and therefore, some antioxidants might be safe as chemoprotectors. Altogether, our studies provide consistent evidence of the beneficial effect of CV on animals treated with cisplatin and might encourage clinical trials