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Aging Clin Exp Res ; 17(1): 1-7, 2005 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-15847115


BACKGROUND AND AIMS: The potential influence of impaired oxidative metabolism in the modulation of manifestations in sporadic Alzheimer's disease (AD) has attracted much attention in the last 50 years. Unfortunately, many clinical and experimental results aiming at proving this hypothesis are still controversial. The aim was to study the enzymatic activities of respiratory chain (RC) complexes I through V in three brain areas of a group of patients with definite AD, and to compare the results with a group of normal brains. We simultaneously assessed the lipid peroxidation of the samples as a measure of free radical damage. METHODS: The specific activity of the individual complexes of the RC was measured spectrophotometrically, and the loss of cis-parinaric acid fluorescence was used to determine the chemical process of lipid peroxidation. RESULTS: We were not able to detect differences in any of the analyzed RC enzymatic activities, or in the level of lipid peroxidation between patients with AD and controls. Instead, differences were found in the number of mitochondria and in the intrinsic enzymatic activities of complexes III and IV in various brain areas. CONCLUSIONS: Spectrophotometric enzymatic analyses of respiratory complexes in brain homogenates do not support the primary contribution of mitochondrial RC dysfunction in the pathogenesis of AD.

Doença de Alzheimer/metabolismo , Encéfalo/metabolismo , Mitocôndrias/metabolismo , Idoso , Idoso de 80 Anos ou mais , Estudos de Casos e Controles , Transporte de Elétrons , Complexo III da Cadeia de Transporte de Elétrons/metabolismo , Complexo IV da Cadeia de Transporte de Elétrons/metabolismo , Feminino , Humanos , Peroxidação de Lipídeos , Masculino , Bancos de Tecidos , Distribuição Tecidual
Med Sci Monit ; 10(9): CS49-53, 2004 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-15328490


BACKGROUND: The enzymatic analysis of mitochondrial respiratory chain (MRC) complexes of skeletal muscle is an important step in the diagnosis of mitochondrial disorders. Because of its lesser turbidity and increased sensitivity, mitochondrial fractionation has been increasingly considered the diagnostic method of choice compared with the more classical analysis of muscle homogenate. In circumstances in which mitochondria become abnormal in number, size or shape, the process of mitochondrial enrichment made by sequential centrifugation and washing may favor the selection of the most normal mitochondria, eliminating the most abnormal ones. In this situation, the study of muscle homogenate, paradoxically, may better reflect what happens in vivo. CASE REPORT: To exemplify this situation we present a 60-year-old woman with a complete mitochondrial phenotype and a 70% heteroplasmic presence of the mtDNA A3243G mutation in muscle tissue. The respiratory and enzymatic activities from mitochondria-enriched muscle suspension were within normal control limits. In contrast, when muscle homogenate was studied, enzyme activities of complexes I, III, and V were found to be decreased. CONCLUSIONS: Although mitochondria-enriched muscle suspensions are usually more informative than muscle homogenates for studies of MRC, in some situations it may be necessary to study both to uncover the biochemical defect.

Miopatias Mitocondriais , Músculo Esquelético/citologia , Músculo Esquelético/fisiopatologia , Fosforilação Oxidativa , Biópsia , Encéfalo/diagnóstico por imagem , Encéfalo/patologia , Fracionamento Celular , DNA Mitocondrial/análise , Transporte de Elétrons , Complexo de Proteínas da Cadeia de Transporte de Elétrons/genética , Complexo de Proteínas da Cadeia de Transporte de Elétrons/metabolismo , Feminino , Humanos , Pessoa de Meia-Idade , Mitocôndrias/enzimologia , Mitocôndrias/genética , Mitocôndrias/ultraestrutura , Miopatias Mitocondriais/diagnóstico , Miopatias Mitocondriais/enzimologia , Miopatias Mitocondriais/patologia , Miopatias Mitocondriais/fisiopatologia , Músculo Esquelético/metabolismo , Músculo Esquelético/patologia , Radiografia , Extratos de Tecidos/química , Extratos de Tecidos/metabolismo
Med Clin (Barc) ; 122(11): 401-6, 2004 Mar 27.
Artigo em Espanhol | MEDLINE | ID: mdl-15066246


BACKGROUND AND OBJECTIVE: Many experimental studies in animals have demonstrated that carbon monoxide (CO) has the ability to bind to complex IV of the mitochondrial respiratory chain (MRC) inhibiting its function. It is unknown, however, if this situation is also present in patients who are admitted to an emergency department because of acute CO poisoning. The objective of this study was to evaluate from different points of view whether or not mitochondrial function is abnormal in patients admitted because of an acute CO poisoning. PATIENTS AND METHOD: Ten patients with an acute CO poisoning admitted in an emergency department were included in the study. Initial carboxyhemoglobin was 20.4 (6)%. Seven of these patients received hyperbaric-oxygen therapy. In all the patients, lymphocytes from 20 mL of blood were obtained at admission (t0), and at days 3-5 (t1), and 10-14 (t2). Mitochondrial content was estimated through citrate synthase activity (nmol/min/mg protein). Enzymatic activity of complexes III and IV (both containing cytochromes) as well as oxidative activities were measured. Lipid peroxidation was ascertained by means of cis-parinaric acid fluorescence. All the values were given as absolute values, and were corrected according to the mitochondrial content (relative values). The results were compared with the control values obtained from 130 historical normal individuals. RESULTS: During acute poisoning (t0), there were no changes in mitochondrial content. On the other hand, there was a significant inhibition of the enzymatic activity of complexes III and IV, and a decrease in all oxidative activities, considering both absolute and relative values. Although all the activities showed a trend to recuperation with time (t1 y t2), statistical significance was only observed for complex IV and for the oxydative activity stimulated with glutamate. CONCLUSIONS: In the present study we confirm that an inhibition of the MRC can be demonstrated ex vivo in patients attended in an emergency department due to acute CO poisoning. The inhibition is still present 14 days after the acute event. This mitochondrial dysfunction may play a pathogenic role in the persisting or delayed sings and symptoms that these patients occasionally refer.

Intoxicação por Monóxido de Carbono/metabolismo , Mitocôndrias/fisiologia , Adulto , Intoxicação por Monóxido de Carbono/fisiopatologia , Emergências , Feminino , Humanos , Masculino