Differential investigation of the capacity of succinate oxidation in human skeletal muscle

Fischer, Johan; Ruitenbeek, W.; Berden, J.A.; Trijbels, J. M. F.; Veerkamp, J.H.; Stadhouders, A. M.; Sengers, R. C. A.; Janssen, A.J.M.

doi:10.1016/0009-8981(85)90135-4

Cited by 427 publications

(190 citation statements)

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“…Succinate dehydrogenase activity was determined as per Fischer et al, 18 measured by following the decrease in absorbance due to reduction of 2,6-di-chloro-indophenol (2,6-DCIP) at 600 nm with 700 nm as reference wavelength (e = 19.1 mM -1 cm -1 ) in the presence of phenazine methosulphate (PMS). The reaction mixture consisting of 40 mM potassium phosphate, pH 7.4, 16 mM succinate, and 8 mM 2,6-DCIP was pre-incubated with 40-80 mg homogenate protein at 30 6C for 20 min.…”

Section: Succinate Dehydrogenasementioning

confidence: 99%

“…The activity of succinate-2,6-dichloroindophenol (DCIP)-oxidoreductase (complex II) was determined by the method described by Fischer et al 18 Complex II activity was measured by following the decrease in absorbance due to reduction of 2,6-DCIP at 600 nm.…”

Section: Complex IImentioning

confidence: 99%

“…The activity of succinate: cytochrome c oxidoreductase (complex III) was determined by the method described by Fischer et al 18 Complex II-III activity was measured by cytochrome c reduction using succinate as substrate at 550 nm.…”

Section: Complex Ii-iiimentioning

confidence: 99%

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Fluvoxamine alters the activity of energy metabolism enzymes in the brain

Ferreira

Cardoso

Jeremias

et al. 2014

Rev. Bras. Psiquiatr.

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Objective: Several studies support the hypothesis that metabolism impairment is involved in the pathophysiology of depression and that some antidepressants act by modulating brain energy metabolism. Thus, we evaluated the activity of Krebs cycle enzymes, the mitochondrial respiratory chain, and creatine kinase in the brain of rats subjected to prolonged administration of fluvoxamine. Methods: Wistar rats received daily administration of fluvoxamine in saline (10, 30, and 60 mg/kg) for 14 days. Twelve hours after the last administration, rats were killed by decapitation and the prefrontal cortex, cerebral cortex, hippocampus, striatum, and cerebellum were rapidly isolated. Results: The activities of citrate synthase, malate dehydrogenase, and complexes I, II-III, and IV were decreased after prolonged administration of fluvoxamine in rats. However, the activities of complex II, succinate dehydrogenase, and creatine kinase were increased. Conclusions: Alterations in activity of energy metabolism enzymes were observed in most brain areas analyzed. Thus, we suggest that the decrease in citrate synthase, malate dehydrogenase, and complexes I, II-III, and IV can be related to adverse effects of pharmacotherapy, but long-term molecular adaptations cannot be ruled out. In addition, we demonstrated that these changes varied according to brain structure or biochemical analysis and were not dose-dependent.

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Section: Succinate Dehydrogenasementioning

confidence: 99%

Section: Complex IImentioning

confidence: 99%

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Fluvoxamine alters the activity of energy metabolism enzymes in the brain

Ferreira

Cardoso

Jeremias

et al. 2014

Rev. Bras. Psiquiatr.

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“…A atividade da SDH foi verificada utilizado o sistema 2,6-DCIP em 600nm na presença de metassulfato de fenazina, segundo o método de Fischer et al (8) .…”

Section: Succcinato Desidrogenaseunclassified

“…A atividade enzimática foi medida pelo método descrito por Fischer et al (8) , onde a diminuição da absorbância do 2,6-DCIP em 600nm é usada para o cálculo da atividade do complexo II.…”

Section: Atividade Do Complexo IIunclassified

Comparação do treinamento físico de quatro e oito semanas sobre atividade da cadeia transportadora de elétrons e marcadores de estresse oxidativo em fígado de camundongos

Silva

Ronsani

Souza

et al. 2010

Rev Bras Med Esporte

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RESUMOO presente estudo investigou o efeito de quatro e oito semanas de treinamento físico sobre a atividade dos complexos da cadeia transportadora de elétrons (CTE) e os marcadores de estresse oxidativo em fígado de camundongos. Vinte e um camundongos (CF1, 30-35g) foram distribuídos nos seguintes grupos: não treinado (NT); treinado quatro semanas (T4); treinado oito semanas (T8). Quarenta e oito horas após a última sessão de treinamento os animais foram mortos por decapitação e o fígado foi retirado e estocado em -70ºC para posterior análise. Atividade da succinato desidrogenase (SDH), dos complexos I,II,III e IV da CTE, carbonilação de proteína, conteúdo total de tióis e a atividade da superóxido dismutase foram mensurados. Os resultados demonstram que apenas oito semanas de treinamento aumentam a atividade da SDH, dos quatro complexos da CTE, da superóxido dismutase, e o conteúdo total de tióis em relação ao grupo não treinado. Houve ainda diminuição na carbonilação de proteína no respectivo grupo em relação ao NT. Em conclusão, são necessárias oito semanas de treinamento para que ocorram aumento no funcionamento mitocondrial e melhora nos marcadores de estresse oxidativo em fígado de camundongos. Palavras-chave: treinamento físico, cadeia transportadora de elétrons, estresse oxidativo ABSTRACTThe present study investigated mitochondrial adaptations and oxidative stress markers after four and eight weeks of running training in liver of mice. Twenty-one male mice (CF1, 30-35g) were distributed into the following groups (n=7): untrained (UT); trained -four weeks (T4); trained -eight weeks (T8). Forty-eight hours after the last training session the animals were killed by decapitation and livers were removed and stored at -70ºC. Succinate dehydrogenase (SDH), complexes I, II, II-III and IV, protein carbonyls (PC), total thiol content and superoxide dismutase activity were measured. The results show that endurance training (8-wk) increases the SDH activity and complexes (I, II, III, IV), superoxide dismutase and total thiol content in liver when compared to untrained animals. Decrease in protein carbonylation in the respective group in relation to UT was also observed. It could be concluded that eight weeks of running training are necessary for mitochondrial respiratory chain enzyme activities increase and improvement in oxidative stress markers in liver of mice.Keywords: physical training, electron transport chain, oxidative stress INTRODUÇÃOEstudos têm reportado que o exercício físico aumenta a produção das espécies reativas de oxigênio (ERO) e, consequentemente, estresse oxidativo em diversos órgãos e tecidos (1,2) . Tem sido sugerido que a elevação do consumo de oxigênio induzida pelos exercícios aumenta a atividade mitocondrial, gerando altas concentrações de ERO (3) . O estresse oxidativo (EO) altera a integridade de constituintes celulares e compromete todo o funcionamento celular (1) . Células hepáticas precisam de energia para realizar diversas funções. A alta taxa metabólica do fígado (200kcal/kg/tecido...

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