RESUMO
Introducción. La persona con insuficiencia cardiaca enfrenta cambios biopsicosociales que deterioran su calidad de vida. Es necesario conocer la relación existente entre el autocuidado y la calidad de vida, lo que puede orientar al profesional de enfermería en el diseño de intervenciones efectivas. Objetivo. Determinar la relación existente entre la capacidad de agencia de autocuidado y la calidad de vida relacionada con la salud en las personas con insuficiencia cardiaca, que son atendidas en el programa multidisciplinario de insuficiencia cardiaca en una institución de salud de cuarto nivel en Bogotá, Colombia. Método. Estudio descriptivo correlacional de corte transversal, realizado entre mayo y agosto de 2018; utilizando los instrumentos Appraisal of Self-care Agency Scale y el Cuestionario de Cardiomiopatía de Kansas City; la muestra correspondió a 107 pacientes, mayores de edad, con insuficiencia cardiaca estadio C y D. Resultados. La capacidad de agencia de autocuidado se encontró en categorías alta con 63,55% y muy alta con 34,57%; la calidad de vida relacionada con la salud se encontró preservada, con un puntaje general de 73,33; la relación existente entre las dos variables, según el coeficiente de correlación de Spearman, fue 0,316 con un valor p = 0,002, relación débil pero significativa. Conclusiones. Existe una relación entre las variables de interés, que se reafirma con las correlaciones significativas identificadas entre las dimensiones que las conforman. Estos hallazgos resaltan la pertinencia de abordar, en las intervenciones, temáticas que fortalezcan la capacidad de agencia de autocuidado, contribuyendo a mejorar la calidad de vida de estas personas.
Introduction. The person with heart failure faces biopsychosocial changes that impair their quality of life. It is necessary to know the relationship between self-care and quality of life, which can guide the nursing professional in the design of effective interventions. Objective. To determine the relationship between the capacity of self-care agency and health-related quality of life in people with heart failure who are treated in the multidisciplinary program of heart failure in a fourth level health institution in Bogotá, Colombia. Method. Descriptive study correlational, cross-sectional, made between May and August 2018; using the Appraisal of Self-care agency Scale Instruments and the Kansas City Cardiomyopathy Questionnaire; the sample corresponded to 107 patients, of legal age, with stage C and D heart failure. Results. The capacity of self-care agency was in high category with 63.55% and very high with 34.57%; the health-related quality of life was preserved, with an overall score of 73.33; the relationship between the two variables, according to the Spearman correlation coefficient, was 0.316 with a value p = 0.002, a weak but significant relationship. Conclusions. There is a relationship between the variables of interest, which is reaffirmed with the significant correlations identified between the dimensions that comprise them. These findings highlight the relevance of addressing, in the interventions, issues that strengthen the capacity of self-care agency, contributing to improve the quality of life of these people.
Introdução. A pessoa com insuficiência cardíaca enfrenta mudanças biopsicossociais deteriorando sua qualidade de vida. É preciso conhecer a relação existente entre autocuidado e qualidade de vida, o que pode nortear o profissional de enfermagem no desenho de intervenções eficazes. Objetivo. Determinar a relação entre a capacidade de agência de autocuidado e a qualidade de vida relacionada à saúde em pessoas com insuficiência cardíaca, tratadas no programa multidisciplinar de insuficiência cardíaca numa instituição de saúde de quarto nível em Bogotá, Colômbia. Método. Estudo descritivo correlacional transversal, realizado entre maio e agosto de 2018; utilizando os instrumentos Appraisal of Self-care Agency Scale e o Questionário de Cardiomiopatia de Kansas City; a amostra correspondeu a 107 pacientes, maiores de idade, com insuficiência cardíaca estagio C e D. Resultados. A capacidade de agência de autocuidado achou-se em categorias alta com 63,55% e muito alta com 34,57%; a qualidade de vida relacionada à saúde encontrou-se preservada, com escore geral de 73,33; a relação entre as duas variáveis, conforme o coeficiente de correlação de Spearman, foi 0,316 com valor p = 0,002, relação fraca, mas significativa. Conclusões. Existe relação entre as variáveis de interesse, o que se reafirma com as correlações significativas identificadas entre as dimensões que as compõem. Esses achados ressaltam a relevância de abordar, nas intervenções, questões que fortaleçam a capacidade de agência de autocuidado, contribuindo a melhorar a qualidade de vida dessas pessoas.
Assuntos
Humanos , Qualidade de Vida , Autocuidado , Insuficiência CardíacaRESUMO
El presente estudio, de tipo cuantitativo correlacional, tiene como objetivo determinar la relación existente entre la capacidad de agencia de autocuidado y la calidad de vida relacionada con la salud en las personas con insuficiencia cardiaca que son atendidos en el programa multidisciplinario de insuficiencia cardiaca de una institución de salud de cuarto nivel en la ciudad de Bogotá, Colombia. La muestra correspondió a 107 pacientes. Las variables se midieron a través de los instrumentos Appraisal of self-care agency scale y el Cuestionario de cardiomiopatía de Kansas City. Resultados: La media de la edad fue 59.9 años, el 66.3% se encontró en la categoría de 51 a 75 años. El sexo masculino predominó con un 67.3%. La ocupación independiente obtuvo el mayor porcentaje. El nivel educativo fue 17.8% en bachillerato completo y universitario. La etiología más común fue isquémica con 40.18%. La clase funcional NYHA estuvo en clase I y II con 27.10% y 61.68% respectivamente. La FEVI fue <40% en el 84.11%. La capacidad de agencia de autocuidado se encontró en categorías alto con 63.55% y muy alto con 34.57%. La calidad de vida relacionada con la salud se encontró preservada, con un puntaje general de 73.33. La relación existente entre las dos variables (coeficiente de correlación de Spearman) fue 0.316 con un p=0.002, relación débil pero significativa. Los resultados del estudio ratifican la necesidad de generar propuestas de intervención de enfermería que evalúen estas variables y contribuyan a la atención integral de las personas con insuficiencia cardiaca.
The objective of this study, which is of a correlational quantitative, is to determine the relationship between self-care agency capacity and the quality of life related to health in people with heart failure who are treated in the multidisciplinary heart failure program of a fourth level health institution in the city of Bogotá, Colombia. The sample corresponded to 107 patients. The variables were measured through the Appraisal of self-care agency scale instruments and the Cardiomyopathy Questionnaire of Kansas City. Results: The mean age was 59.9 years, 66.3% was found in the category of 51 to 75 years. Male sex predominated with 67.3%. Independent occupation obtained the highest percentage. The educational level was 17.8% in high school and university. The most common etiology was ischemic with 40.18%. The NYHA functional class was in class I and II with 27.10% and 61.68% respectively. LVEF was < 40% in 84.11%. The self-care agency capacity was found in high categories with 63.55% and very high with 34.57%. The quality of life related to health was slightly affected with a general score of 73.33. The relationship between the two variables (Spearman correlation coefficient) was 0.316 with p = 0.002, a weak but significant relationship. The results of the study confirm the need to generate nursing intervention proposals that evaluate these variables and contribute to the comprehensive care of people with heart failure.
Assuntos
Humanos , Masculino , Feminino , Qualidade de Vida , Autocuidado , Insuficiência CardíacaRESUMO
The chemotherapeutic drug cisplatin has some side effects including nephrotoxicity that has been associated with reactive oxygen species production, particularly superoxide anion. The major source of superoxide anion is nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) oxidase. However, the specific segment of the nephron in which superoxide anion is produced has not been identified. Rats were sacrificed 72 h after cisplatin injection (7.5 mg/kg), and kidneys were obtained to isolate glomeruli and proximal and distal tubules. Cisplatin induced superoxide anion production in glomeruli and proximal tubules but not in distal tubules. This enhanced superoxide anion production was prevented by diphenylene iodonium, an inhibitor of NADPH oxidase. Consistently, this effect was associated with the increased expression of gp91(phox) and p47(phox), subunits of NADPH oxidase. The enhanced superoxide anion production in glomeruli and proximal tubules, associated with the increased expression of gp91(phox) and p47(phox), is involved in the oxidative stress in cisplatin-induced nephrotoxicity.
Assuntos
Antineoplásicos/toxicidade , Cisplatino/toxicidade , Glomérulos Renais/efeitos dos fármacos , Túbulos Renais Proximais/efeitos dos fármacos , Glicoproteínas de Membrana/metabolismo , NADPH Oxidases/metabolismo , Superóxidos/metabolismo , Animais , Glomérulos Renais/metabolismo , Túbulos Renais Proximais/metabolismo , Masculino , NADPH Oxidase 2 , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos WistarRESUMO
Excitotoxicity and oxidative stress are mechanisms involved in the neuronal cell death induced by the intrastriatal injection of quinolinic acid (QUIN) as a model of Huntington's disease. Production of nitric oxide by nitric oxide synthase (NOS) has been proposed to participate in QUIN-induced neurotoxicity; however, the precise role of NOS in QUIN-induced toxicity still remains controversial. In order to provide further information on the role of NOS isoforms in QUIN toxicity, we performed real time RT-PCR and immunohistochemistry of inducible NOS (iNOS), endothelial NOS (eNOS) and neuronal NOS (nNOS) and determined Ca(2+)-dependent and Ca(2+)-independent NOS activity in a temporal course (3-48h), after an intrastriatal injection of QUIN to rats. NOS isoforms exhibited a transitory expression of mRNA and protein after QUIN infusion: eNOS increased between 3 and 24h, iNOS between 12 and 24h, while nNOS at 35 and 48h. Ca(2+)-independent activity (iNOS) did not show any change, while Ca(2+)-dependent activity (constitutive NOS: eNOS/nNOS) exhibited increased levels at 3h. Our results support the participation of Ca(2+)-dependent NOS isoforms during the toxic events produced at early times after QUIN injection.
Assuntos
Gânglios da Base/enzimologia , Regulação Enzimológica da Expressão Gênica , Doença de Huntington/enzimologia , Óxido Nítrico Sintase Tipo II/metabolismo , Óxido Nítrico Sintase/metabolismo , Óxido Nítrico/metabolismo , Animais , Cálcio/metabolismo , Modelos Animais de Doenças , Doença de Huntington/induzido quimicamente , Imuno-Histoquímica , Masculino , Óxido Nítrico Sintase/genética , Óxido Nítrico Sintase Tipo I , Óxido Nítrico Sintase Tipo II/genética , Óxido Nítrico Sintase Tipo III , Ácido Quinolínico , RNA Mensageiro/metabolismo , Ratos , Ratos Wistar , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fatores de Tempo , Regulação para CimaRESUMO
Reactive oxygen and nitrogen species formation leads to DNA damage in animals treated with quinolinic acid. Poly(ADP-ribose) polymerase-1 (PARP-1) is a protein involved in the DNA base excision repair system. Its overactivation promotes cellular energy deficit and necrosis. Here, we evaluated the effect of PJ-34, a potent inhibitor of PARP-1, on the neuronal damage induced by quinolinic acid. Animals were administered with PJ-34 (10 mg/kg, i.p.), 1 h before and 1 h after a striatal infusion of 1 microl of quinolinic acid (240 nmol). PJ-34 clearly attenuated the circling behavior produced by quinolinic acid and completely prevented the histological damage induced by the toxin. The protective effect of PJ-34 suggests that PARP-1 activation is playing an active role in the neuronal death induced by quinolinic acid.
Assuntos
Neurônios/efeitos dos fármacos , Poli(ADP-Ribose) Polimerases/metabolismo , Ácido Quinolínico/farmacologia , Animais , Comportamento Animal/efeitos dos fármacos , Encéfalo/citologia , Morte Celular/efeitos dos fármacos , Interações Medicamentosas , Inibidores Enzimáticos/farmacologia , Masculino , Fenantrenos/farmacologia , Ratos , Ratos Wistar , Comportamento Estereotipado/efeitos dos fármacosRESUMO
It has been found that S-allylcysteine (SAC), a garlic-derived compound, has in vivo and in vitro antioxidant properties. In addition, it is known that SAC is able to scavenge different reactive oxygen or nitrogen species including superoxide anion (O(2)(-)), hydrogen peroxide (H(2)O(2)), hydroxyl radical (OH()), and peroxynitrite anion (ONOO(-)) although the IC(5O) values for each reactive species has not been calculated and the potential ability of SAC to scavenge singlet oxygen ((1)O(2)) and hypochlorous acid (HOCl) has not been explored. The purposes of this work was (a) to explore the potential ability of SAC to scavenge (1)O(2) and HOCl, (b) to further characterize the O(2)(-), H(2)O(2), OH(), and ONOO(-) scavenging ability of SAC by measuring the IC(50) values using in vitro assays, and (c) to explore the potential ability of SAC to ameliorate the potassium dichromate (K(2)Cr(2)O(7))-induced cytotoxicity in LLC-PK1 cells in which oxidative stress is involved. The scavenging activity was compared against the following reference compounds: N-acetylcysteine for O(2)(-), sodium pyruvate for H(2)O(2), dimethylthiourea for OH(), lipoic acid and glutathione for (1)O(2), lipoic acid for HOCl, and penicillamine for ONOO(-). It was found that SAC was able to scavenge concentration-dependently all the species assayed with the following IC(5O) (mean+/-SEM, mM): O(2)(-) (14.49+/-1.67), H(2)O(2) (68+/-1.92), OH() (0.68+/-0.06), (1)O(2) (1.93+/-0.27), HOCl (2.86+/-0.15), and ONOO(-) (0.80+/-0.05). When the ability of SAC to scavenge these species was compared to those of the reference compounds it was found that the efficacy of SAC (a) to scavenge O(2)(-), H(2)O(2), OH(), and ONOO(-) was lower, (b) to scavenge HOCl was similar, and (c) to scavenge (1)O(2) was higher. In addition, it was found that SAC was able to prevent K(2)Cr(2)O(7)-induced toxicity in LLC-PK1 cells in culture. It was showed for the first time that SAC is able to scavenge (1)O(2) and HOCl and to ameliorate the K(2)Cr(2)O(7)-induced toxicity.
Assuntos
Cisteína/análogos & derivados , Sequestradores de Radicais Livres , Ácido Hipocloroso/química , Dicromato de Potássio/antagonistas & inibidores , Dicromato de Potássio/toxicidade , Espécies Reativas de Oxigênio/química , Animais , Sobrevivência Celular/efeitos dos fármacos , Cisteína/farmacologia , Peróxido de Hidrogênio/química , Radical Hidroxila/química , Células LLC-PK1 , Ácido Pirúvico/metabolismo , Superóxidos/química , Suínos , Ácido Tióctico/metabolismo , Tioureia/análogos & derivados , Tioureia/metabolismoRESUMO
Se realizó una investigación-acción participativa en 32 niños en edad escolar, con conductas agresivas, del Colegio General Santander de Chía, para observar cómo influye el medio familiar y escolar en las conductas agresivas de los niños, y plantear alternativas para modular dichas conductas. El estudio indagó, en niños y padres de familia, factores determinantes de las conductas agresivas. Se evaluaron el tipo de estructura familiar, las personas responsables del cuidado de los niños, las condiciones de vivienda, el hacinamiento, el nivel de escolaridad, la situación laboral, los métodos correctivos y el consumo de alcohol por parte de los padres o cuidadores, como variables determinantes del medio familiar. Se encontró que los determinantes que influyeron en las manifestaciones agresivas de los niños, en este caso, fueron: el tipo de estructura familiar, el bajo nivel de escolaridad de los padres, y las personas responsables de la educación y cuidado de los niños; y en relación con el medio escolar, la fuente de imitación de conductas agresivas.
Assuntos
Comportamento , PesquisaRESUMO
Gentamicin (GM)-induced nephrotoxicity limits the use of this antibiotic. It has been shown that aged garlic extract (AGE) and S-allylcysteine (SAC), the most abundant organosulfur compound in AGE, ameliorate GM-induced nephrotoxicity in rats. The present communication evaluated the effect of AGE and SAC on proliferation and on GM-induced toxicity and genotoxicity of porcine kidney epithelial cell line (LLC-PK1 cells). The cells were preincubated with different concentrations of AGE or SAC for 12 h before incubation with 8 mm GM for an additional 72 h. At the end of this time, cell viability, genotoxicity and proliferation were evaluated. AGE stimulated cell proliferation and protected LLC-PK1 cells from GM-mediated toxicity and genotoxicity. SAC partially prevented only GM-induced genotoxicity. These results suggest that the stimulation of cell proliferation could possibly be one of the mechanisms involved in the in vitro protective effect of AGE in GM-induced toxicity of LLC-PK1 cells.
Assuntos
Antibacterianos/toxicidade , Cisteína/análogos & derivados , Alho , Gentamicinas/toxicidade , Extratos Vegetais/farmacologia , Substâncias Protetoras/farmacologia , Análise de Variância , Animais , Bromodesoxiuridina/metabolismo , Proliferação de Células/efeitos dos fármacos , Cisteína/farmacologia , Relação Dose-Resposta a Droga , Interações Medicamentosas , Ensaio de Imunoadsorção Enzimática , Alho/química , Células LLC-PK1 , Testes de Mutagenicidade , Fitoterapia , Testes de ToxicidadeRESUMO
Se realizó una investigación-acción participativa en 32 niños en edad escolar, con conductas agresivas, del Colegio General Santander de Chía, para observar cómo influye el medio familiar y escolar en las conductas agresivas de los niños, y plantear alternativas para modular dichas conductas. El estudio indagó, en niños y padres de familia, factores determinantes de las conductas agresivas. Se evaluaron el tipo de estructura familiar, las personas responsables del cuidado de los niños, las condiciones de vivienda, el hacinamiento, el nivel de escolaridad, la situación laboral, los métodos correctivos y el consumo de alcohol por parte de los padres o cuidadores, como variables determinantes del medio familiar. Se encontró que los determinantes que influyeron en las manifestaciones agresivas de los niños, en este caso, fueron: el tipo de estructura familiar, el bajo nivel de escolaridad de los padres, y las personas responsables de la educación y cuidado de los niños; y en relación con el medio escolar, la fuente de imitación de conductas agresivas
Assuntos
Humanos , Educação , Educação/estatística & dados numéricos , Educação/ética , Valores Sociais , Estudantes , Maus-Tratos InfantisRESUMO
BACKGROUND: It has been established that hypothyroidism protects rats against renal ischemia and reperfusion (IR) oxidative damage. However, it is not clear if hypothyroidism is able to prevent protein tyrosine nitration, an index of nitrosative stress, induced by IR or if antioxidant enzymes have involved in this protective effect. In this work it was explored if hypothyroidism is able to prevent the increase in nitrosative and oxidative stress induced by IR. In addition the activity of the antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase was studied. Control and thyroidectomized (HTX) rats were studied 24 h of reperfusion after 60 min ischemia. METHODS: Male Wistar rats weighing 380 +/- 22 g were subjected to surgical thyroidectomy. Rats were studied 15 days after surgery. Euthyroid sham-operated rats were used as controls (CT). Both groups of rats underwent a right kidney nephrectomy and suffered a 60 min left renal ischemia with 24 h of reperfusion. Rats were divided in four groups: CT, HTX, IR and HTX+IR. Rats were sacrificed and samples of plasma and kidney were obtained. Blood urea nitrogen (BUN) and creatinine were measured in blood plasma. Kidney damage was evaluated by histological analysis. Oxidative stress was measured by immunohistochemical localization of protein carbonyls and 4-hydroxy-2-nonenal modified proteins. The protein carbonyl content was measured using antibodies against dinitrophenol (DNP)-modified proteins. Nitrosative stress was measured by immunohistochemical analysis of 3-nitrotyrosine modified proteins. The activity of the antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase was measured by spectrophotometric methods. Multiple comparisons were performed with ANOVA followed by Bonferroni t test. RESULTS: The histological damage and the rise in plasma creatinine and BUN induced by IR were significantly lower in HTX+IR group. The increase in protein carbonyls and in 3-nitrotyrosine and 4-hydroxy-2-nonenal modified proteins was prevented in HTX+IR group. IR-induced decrease in renal antioxidant enzymes was essentially not prevented by HTX in HTX+IR group. CONCLUSION: Hypothyroidism was able to prevent not only oxidative but also nitrosative stress induced by IR. In addition, the antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase seem not to play a protective role in this experimental model.
Assuntos
Hipotireoidismo/complicações , Rim/irrigação sanguínea , Rim/patologia , Estresse Oxidativo , Oxirredutases/metabolismo , Traumatismo por Reperfusão/patologia , Tirosina/análogos & derivados , Animais , Catalase/metabolismo , Glutationa Peroxidase/metabolismo , Imuno-Histoquímica , Rim/metabolismo , Masculino , Ratos , Ratos Wistar , Traumatismo por Reperfusão/complicações , Traumatismo por Reperfusão/metabolismo , Superóxido Dismutase/metabolismo , Tirosina/metabolismoRESUMO
BACKGROUND: Potassium dichromate (K2Cr2O7)-induced nephrotoxicity is associated with oxidative and nitrosative stress. In this study we investigated the relation between the time course of the oxidative and nitrosative stress with kidney damage and alterations in the following antioxidant enzymes: Cu, Zn superoxide dismutase (Cu, Zn-SOD), Mn-SOD, glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT). METHODS: Nephrotoxicity was induced in rats by a single injection of K2Cr2O7. Groups of animals were sacrificed on days 1,2,3,4,6,8,10, and 12. Nephrotoxicity was evaluated by histological studies and by measuring creatinine clearance, serum creatinine, blood urea nitrogen (BUN), and urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) and total protein. Oxidative and nitrosative stress were measured by immunohistochemical localization of protein carbonyls and 3-nitrotyrosine, respectively. Cu, Zn-SOD, Mn-SOD, and CAT were studied by immunohistochemical localization. The activity of total SOD, CAT, GPx, and GR was also measured as well as serum and kidney content of chromium and urinary excretion of NO2 -/NO3-. Data were compared by two-way analysis of variance followed by a post hoc test. RESULTS: Serum and kidney chromium content increased reaching the highest value on day 1. Nephrotoxicity was made evident by the decrease in creatinine clearance (days 1-4) and by the increase in serum creatinine (days 1-4), BUN (days 1-6), urinary excretion of NAG (days 1-4), and total protein (day 1-6) and by the structural damage to the proximal tubules (days 1-6). Oxidative and nitrosative stress were clearly evident on days 1-8. Urinary excretion of NO2-/NO3- decreased on days 2-6. Mn-SOD and Cu, Zn-SOD, estimated by immunohistochemistry, and total SOD activity remained unchanged. Activity of GPx decreased on days 3-12 and those of GR and CAT on days 2-10. Similar findings were observed by immunohistochemistry of CAT. CONCLUSION: These data show the association between oxidative and nitrosative stress with functional and structural renal damage induced by K2Cr2O7. Renal antioxidant enzymes were regulated differentially and were not closely associated with oxidative or nitrosative stress or with kidney damage. In addition, the decrease in the urinary excretion of NO2-/NO3- was associated with the renal nitrosative stress suggesting that nitric oxide was derived to the formation of reactive nitrogen species involved in protein nitration.
Assuntos
Nefropatias/induzido quimicamente , Nefropatias/metabolismo , Compostos de Nitrogênio/metabolismo , Estresse Oxidativo , Oxirredutases/metabolismo , Dicromato de Potássio , Acetilglucosaminidase/urina , Animais , Catalase/metabolismo , Cromo/sangue , Cromo/metabolismo , Creatina/sangue , Creatina/urina , Glutationa Peroxidase/metabolismo , Imuno-Histoquímica , Rim/efeitos dos fármacos , Rim/metabolismo , Nefropatias/patologia , Túbulos Renais Proximais/patologia , Masculino , Nitratos/urina , Nitritos/urina , Dicromato de Potássio/intoxicação , Proteinúria/fisiopatologia , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismoAssuntos
Encefalopatias/metabolismo , Ferro/metabolismo , Metaloporfirinas/metabolismo , Ácido Peroxinitroso/metabolismo , Ácido Quinolínico/toxicidade , Tirosina/análogos & derivados , Animais , Antioxidantes/metabolismo , Encefalopatias/induzido quimicamente , Corpo Estriado/efeitos dos fármacos , Corpo Estriado/metabolismo , Masculino , Neurotoxinas/toxicidade , Nitrogênio/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos Wistar , Tirosina/metabolismoRESUMO
It has been shown that reactive oxygen species are involved in chronic puromycin aminonucleoside (PAN) induced nephrotic syndrome (NS) and that a 20% soy protein diet reduces renal damage in this experimental model. The purpose of the present work was to investigate if a 20% soy protein diet is able to modulate kidney nitrotyrosine formation and the activity of renal antioxidant enzymes (catalase, glutathione peroxidase, Cu,Zn- or Mn-superoxide dismutase) which could explain, at least in part, the protective effect of the soy protein diet in rats with chronic NS induced by PAN. Four groups of rats were studied: (1) Control rats fed 20% casein diet, (2) Nephrotic rats fed 20% casein diet, (3) Control rats fed 20% soy protein diet, and (4) Nephrotic rats fed 20% soy protein diet. Chronic NS was induced by repeated injections of PAN and rats were sacrificed at week nine. The soy protein diet ameliorated proteinuria, hypercholesterolemia, and the increase in serum creatinine and blood urea nitrogen observed in nephrotic rats fed 20% casein diet. Kidney nitrotyrosine formation increased in nephrotic rats fed 20% casein diet and this increase was ameliorated in nephrotic rats fed 20% soy protein diet. However, the soy protein diet was unable to modulate the antioxidant enzymes activities in control and nephrotic rats fed 20% soy protein diet. Food intake was similar in the two diet groups. The protective effect of a 20% soy protein diet on renal damage in chronic nephropathy induced by PAN was associated with the amelioration in the renal nitrotyrosine formation but not with the modulation of antioxidant enzymes.
Assuntos
Antimetabólitos/toxicidade , Glycine max/química , Falência Renal Crônica/induzido quimicamente , Falência Renal Crônica/prevenção & controle , Rim/metabolismo , Puromicina Aminonucleosídeo/toxicidade , Proteínas de Soja/farmacologia , Tirosina/análogos & derivados , Tirosina/metabolismo , Animais , Antioxidantes/metabolismo , Nitrogênio da Ureia Sanguínea , Peso Corporal/efeitos dos fármacos , Catalase/metabolismo , Colesterol/sangue , Creatinina/sangue , Dieta , Ingestão de Alimentos/efeitos dos fármacos , Glutationa Peroxidase/metabolismo , Imuno-Histoquímica , Rim/efeitos dos fármacos , Rim/patologia , Falência Renal Crônica/patologia , Testes de Função Renal , Lipídeos/sangue , Masculino , Proteinúria/induzido quimicamente , Proteinúria/metabolismo , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismoRESUMO
Gentamicin (GM) is an antibiotic whose clinical use is limited by its nephrotoxicity. Experimental evidences suggest a role of reactive oxygen species in GM-induced nephrotoxicity. In this work we explored the effect of diallyl sulfide (DAS), a garlic-derived compound with antioxidant properties, on GM-induced nephrotoxicity. Four groups of rats were studied: (1) Control, treated intragastrically with olive oil as a vehicle, (2) GM, treated subcutaneously with GM (125 mg/kg/day for 4 days), (3) DAS, treated intragastrically with DAS (50 mg/kg/day for 4 days), and (4) GM + DAS. Nephrotoxicity was made evident by: (1) the increase in creatinine and blood urea nitrogen in serum, (2) the increase in urinary excretion of N-acetyl-beta-D-glucosaminidase and total protein, and (3) necrosis of proximal tubular cells. These functional and structural alterations were prevented or ameliorated by DAS treatment. In addition, GM increased levels of renal oxidative stress markers nitrotyrosine and protein carbonyl groups which were also ameliorated by DAS in GM + DAS group. The mechanism by which DAS has a protective effect on GM-induced nephrotoxicity may be related, at least in part, to the decrease in oxidative stress in renal cortex.
Assuntos
Compostos Alílicos/química , Gentamicinas/farmacologia , Estresse Oxidativo , Sulfetos/química , Tirosina/análogos & derivados , Acetilglucosaminidase/metabolismo , Animais , Antibacterianos/farmacologia , Antioxidantes/metabolismo , Antioxidantes/farmacologia , Nitrogênio da Ureia Sanguínea , Peso Corporal , Carbono/química , Creatinina/sangue , Creatinina/metabolismo , Imuno-Histoquímica , Rim/efeitos dos fármacos , Córtex Renal/metabolismo , Túbulos Renais/citologia , Masculino , Necrose , Azeite de Oliva , Oxigênio/metabolismo , Óleos de Plantas , Ratos , Ratos Wistar , Espécies Reativas de Oxigênio , Fatores de Tempo , Tirosina/químicaRESUMO
Gentamicin (GM) is an antibiotic whose clinical use is limited by its nephrotoxicity. Experimental evidences suggest a role of reactive oxygen species in GM-induced nephrotoxicity. Therefore, we investigated if aged garlic extract (AGE), an antioxidant, has a protective role in this experimental model. Four groups of male Wistar rats were studied: 1) Control (CT), injected subcutaneously (s.c.) and intraperitoneally (i.p.) with saline, 2) GM, treated s.c. with GM (70 mg/kg/12 hours/4 days), 3) AGE, treated i.p with AGE (1.2 mL/kg/12 hours/6 days), and 4) GM + AGE treated with GM and AGE. The treatment with AGE started two days before the first dose of GM (GM + AGE group) or saline (AGE group). Animals were sacrificed on day 5, and blood, urine, and kidneys were obtained. Nephrotoxicity was made evident by: 1) the increase in blood urea nitrogen and plasma creatinine, 2) the decrease in plasma glutathione peroxidase (GPx) activity and the urinary increase in N-acetyl-beta-D-glucosaminidase activity and total protein, and 3) necrosis of proximal tubular cells. These alterations were prevented or ameliorated by AGE treatment. Furthermore, AGE prevented the GM-induced increase in the renal levels of oxidative stress markers: nitrotyrosine and protein carbonyl groups and the decrease in manganese superoxide dismutase (Mn-SOD), GPx, and glutathione reductase (GR) activities. The protective effect of AGE was associated with the decrease in the oxidative stress and the preservation of Mn-SOD, GPx, and GR activities in renal cortex. These data suggest that AGE may be a useful agent for the prevention of GM-nephrotoxicity.
Assuntos
Antibacterianos/antagonistas & inibidores , Antibacterianos/toxicidade , Sequestradores de Radicais Livres/farmacologia , Alho/química , Gentamicinas/antagonistas & inibidores , Gentamicinas/toxicidade , Nefropatias/induzido quimicamente , Nefropatias/patologia , Estresse Oxidativo/fisiologia , Animais , Antibacterianos/metabolismo , Western Blotting , Peso Corporal/efeitos dos fármacos , Catalase/metabolismo , Gentamicinas/metabolismo , Indicadores e Reagentes , Rim/metabolismo , Córtex Renal/efeitos dos fármacos , Córtex Renal/enzimologia , Glomérulos Renais/patologia , Túbulos Renais/patologia , Masculino , Extratos Vegetais/farmacologia , Ratos , Ratos Wistar , Superóxidos/metabolismo , Micção/efeitos dos fármacosRESUMO
This study determined the in vitro effects of 4-hydroxycoumarin (4-HC) employing the melanoma cell line B16-F10 and the non-malignant fibroblastic cell line B82. 4-HC disorganized the actin cytoskeleton in B16-F10 cells, but not in B82 fibroblasts. Cytoskeletal disorganization correlated with reductions in cell adhesion to four extracellular matrix proteins and inhibition of random motility. 4-HC did not modify cell viability or actin expression, but decreased tyrosine phosphorylation of several proteins in melanoma cells. Because adhesion of tumor cells to extracellular matrix is required during the metastatic process, 4-HC might be useful as an adjuvant therapy for melanoma.
Assuntos
4-Hidroxicumarinas/farmacologia , Actinas/efeitos dos fármacos , Adesão Celular/efeitos dos fármacos , Citoesqueleto/efeitos dos fármacos , Proteínas da Matriz Extracelular/metabolismo , Animais , Movimento Celular/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Citoesqueleto/ultraestrutura , Proteínas da Matriz Extracelular/efeitos dos fármacos , Fibroblastos/citologia , Fibroblastos/efeitos dos fármacos , Fibroblastos/fisiologia , Melanoma Experimental/fisiopatologia , Camundongos , Proteínas de Neoplasias/efeitos dos fármacos , Proteínas de Neoplasias/metabolismo , Fosfotirosina/metabolismo , Células Tumorais CultivadasRESUMO
Tuberculosis is the leading infectious disease in the world. Mycobacterium tuberculosis, the causal agent of this disease, invades macrophages and can replicate inside them. Because invasion of macrophages is a critical step for establishing a mycobacterial infection, there is much interest in understanding the mechanisms for M. tuberculosis entry into macrophages. Complement receptor 3 (CR3) is a heterodimeric surface receptor with multiple binding sites, which can mediate complement-opsonized as well as nonopsonic entrance of M. tuberculosis into macrophages. Here, we describe and discuss the role of CR3 in macrophage[bond]M. tuberculosis interactions. The actual information suggests that CR3 mediates a substantial amount of M. tuberculosis binding to macrophages, but CR3 is not related to the mechanisms that allow mycobacteria to survive and replicate intracellularly. Understanding the mechanisms of macrophage[bond]M. tuberculosis interaction will help developing more effective methods to prevent and treat tuberculosis in the future.
Assuntos
Antígeno de Macrófago 1/metabolismo , Macrófagos/imunologia , Macrófagos/microbiologia , Mycobacterium tuberculosis/imunologia , Mycobacterium tuberculosis/patogenicidade , Animais , Humanos , Camundongos , Fagocitose/fisiologia , Tuberculose/imunologia , Tuberculose/microbiologia , Tuberculose/fisiopatologiaRESUMO
Experimental evidences suggest a role of reactive oxygen species in gentamicin-induced nephropathy in rats. Therefore, we investigated if diallyl disulfide, a garlic-derived compound with antioxidant properties, has a renoprotective effect in this experimental model. Four groups of rats were studied: (1) control, (2) gentamicin treated subcutaneously with gentamicin (70 mg/kg/12 h/4 days), (3) diallyl disulfide treated intragastrically with diallyl disulfide (50 mg/kg/24 h/4 days), and (4) gentamicin + diallyl disulfide treated with gentamicin + diallyl disulfide. Gentamicin induced (a) nephrotoxicity, (b) increase in renal oxidative stress, and (c) decrease in the activity of manganese superoxide dismutase, glutathione peroxidase, and glutathione reductase. Diallyl disulfide ameliorated these changes induced by gentamicin. The mechanism by which diallyl disulfide has a renoprotective effect in gentamicin-induced acute renal failure in rats may be related, at least in part, to the amelioration in the oxidative stress and the preservation in the activity of the antioxidant enzymes in kidney.
Assuntos
Compostos Alílicos/uso terapêutico , Antibacterianos/efeitos adversos , Antioxidantes/uso terapêutico , Dissulfetos/uso terapêutico , Gentamicinas/efeitos adversos , Nefropatias/tratamento farmacológico , Estresse Oxidativo/efeitos dos fármacos , Compostos Alílicos/farmacologia , Animais , Antioxidantes/farmacologia , Biomarcadores/análise , Nitrogênio da Ureia Sanguínea , Dissulfetos/farmacologia , Alho/química , Rim/enzimologia , Rim/metabolismo , Rim/patologia , Nefropatias/induzido quimicamente , Nefropatias/patologia , Masculino , Estresse Oxidativo/fisiologia , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismoRESUMO
Acute renal failure (ARF) is a major complication of gentamicin (GM) treatment, which is effective against gram-negative infections. Since experimental evidence suggests a role of reactive oxygen species (ROS) in GM-induced ARF, in this work we studied the effect of a garlic-derived compound, S-allylcysteine (SAC), which is a free radical scavenger, on GM-induced nephrotoxicity. In rats treated with GM (70 mg/kg/12 h/4 days/s.c.), ARF was evident by the: (i) decrease in creatinine clearance and increase in blood urea nitrogen, (ii) decrease in blood glutathione peroxidase (GPx) activity and increase in urinary excretion of N-acetyl-beta-D-glucosaminidase and total protein, and (iii) necrosis of proximal tubular cells. These alterations were prevented by SAC treatment (250 mg/kg/i.p. 24 h before the first dose of GM and 125 mg/kg/12 h/4 days along GM-treatment). Furthermore, SAC prevented the GM-induced oxidative stress (protein carbonyl groups) and the decrease in manganese superoxide dismutase (Mn-SOD), GPx, and glutathione reductase (GR) activities in renal cortex. In conclusion, SAC ameliorates the GM-induced ARF by a mechanism related, at least in part, to its ability to decrease oxidative stress and to preserve antioxidant enzymes activity in renal cortex.
Assuntos
Antioxidantes/farmacologia , Cisteína/análogos & derivados , Cisteína/farmacologia , Gentamicinas/efeitos adversos , Gentamicinas/farmacologia , Rim/patologia , Estresse Oxidativo , Acetilglucosaminidase/urina , Animais , Antibacterianos/farmacologia , Antioxidantes/química , Antioxidantes/metabolismo , Peso Corporal , Sequestradores de Radicais Livres , Radicais Livres , Alho , Glutationa Peroxidase/sangue , Glutationa Peroxidase/metabolismo , Rim/lesões , Córtex Renal/patologia , Túbulos Renais/patologia , Masculino , Necrose , Extratos Vegetais , Ratos , Ratos Wistar , Espécies Reativas de Oxigênio , Fatores de TempoRESUMO
Heme oxygenase (HO) is the rate-limiting enzyme in the degradation of heme; its inducible isozyme HO-1 protects against some types of acute tissue injury. The expression and functional role of HO-1 in rats with renal injury induced by potassium dichromate (K(2)Cr(2)O(7)) was investigated in this work. Rats were studied 24 h after a single injection of K(2)Cr(2)O(7). To address the possible protective effect of HO-1 in this experimental model, this enzyme was induced by an injection of stannous chloride (SnCl(2)) 12 h before K(2)Cr(2)O(7) administration. The functional role of HO-1 in K(2)Cr(2)O(7) + SnCl(2)-treated animals was tested by inhibiting HO activity with an injection of zinc (II) protoporphyrin IX (ZnPP) 18 h before K(2)Cr(2)O(7). In K(2)Cr(2)O(7)-treated rats: (i) renal HO-1 content, measured by Western blot, increased 2.6-fold; and, (ii) renal nitrotyrosine and protein carbonyl content, markers of oxidative stress, increased 3.5- and 1.36-fold, respectively. Renal damage and oxidative stress were ameliorated and HO-1 content was increased in the K(2)Cr(2)O(7) + SnCl(2) group. The attenuation of renal injury and oxidative stress was lost by the inhibition of HO activity in K(2)Cr(2)O(7) + SnCl(2) + ZnPP-treated animals. Our data suggest that HO-1 overexpression induced by SnCl(2) is responsible for the attenuation of renal damage and oxidative stress induced by K(2)Cr(2)O(7).