Navegando por Palavras-chave "Respiratory chain"

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    Bcl-X-L inhibits Bax-induced alterations in mitochondrial respiration and calcium release
    (Elsevier B.V., 2008-09-12) Teles, Alessandra Vaz Fernandes Fiuza [UNIFESP]; Ureshino, Rodrigo Portes [UNIFESP]; Dorta, Daniel Junqueira [UNIFESP]; Lopes, Guiomar Silva [UNIFESP]; Hsu, Yi-Te; Smaili, Soraya Soubhi [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Med Univ S Carolina
    Apoptosis is a natural cell elimination process involved in a number of physiological and pathological events. This process can be regulated by members of the Bcl-2 family. Bax, a pro-apoptotic member of this family, accelerates cell death, while the pro-survival member, Bcl-X-L, can antagonize the pro-apoptotic function of Bax to promote cell survival. in the present study, we have evaluated the effect of Bcl-X-L on Bax-induced alterations in mitochondrial. respiration and calcium release. We found that in primary cultured astrocytes, recombinant Bcl-X-L is able to antagonize Bax-induced decrease in mitochondrial respiration and increase in mitochondrial. calcium release. in addition, we found that Bcl-X-L can lower the calcium store in the endoplasmic reticulum, thus limiting potential calcium flux induced by apoptosis. This regulation of calcium flux by Bcl-X-L may represent an important mechanism by which this protein promotes cell survival. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
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    Complex I spectrophotometric assay in cultured cells: Detailed analysis of key factors
    (Elsevier B.V., 2013-04-01) Oliveira, Katia Klug [UNIFESP]; Kiyomoto, Beatriz Hitomi [UNIFESP]; Rodrigues, Andresa De Santi [UNIFESP]; Tengan, Celia Harumi [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The diagnosis of mitochondrial encephalomyopathies caused by complex I (C-I) deficiency relies mainly on the spectrophotometric C-I assay. Considered difficult, this assay lacks reliability and has high nonspecific activity. We studied the key factors of this assay in cultured cells (cybrid and fibroblast): ubiquinone analogues, rotenone inhibition to determine specific activity, and mode of permeabilization of mitochondria] membranes. We showed that ubiquinone 1 allows a more stable and reliable assay, better results were obtained with rotenone inhibition done in the same assay, and mitochondria] permeability was improved just by freeze/thawing the sample prior to the assay. (C) 2012 Elsevier Inc. All rights reserved.
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    Neonatal mitochondrial encephaloneuromyopathy due to a defect of mitochondrial protein synthesis
    (Elsevier B.V., 2008-12-15) Ferreiro-Barros, Claudia Cristina [UNIFESP]; Tengan, Celia Harumi [UNIFESP]; Barros, Mario Henrique de; Palenzuela, Lluis; Kanki, Chisaka; Quinzii, Catarina; Lou, Johanna; El Gharaby, Nader; Shokr, Aly; De Vivo, Darryl C.; DiMauro, Salvatore; Hirano, Michio; Columbia Univ; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP); Bugshan Gen Hosp
    Mitochondrial diseases are clinically and genetically heterogeneous disorders due to primary mutations in mitochondrial DNA (mtDNA) or nuclear DNA (nDNA). We studied a male infant with severe congenital encephalopathy, peripheral neuropathy, and myopathy. the patient's lactic acidosis and biochemical defects of respiratory chain complexes I, III, and IV in muscle indicated that he had a mitochondrial disorder while parental consanguinity suggested autosomal recessive inheritance. Cultured fibroblasts from the patient showed a generalized defect of mitochondrial protein synthesis. Fusion of cells from the patient with 143B206 rho(0) cells devoid of mtDNA restored cytochrome c oxidase activity confirming the nDNA origin of the disease. Our studies indicate that the patient has a novel autosomal recessive defect of mitochondrial protein synthesis. (C) 2008 Elsevier B.V. All rights reserved.
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    NO control of mitochondrial function in normal and transformed cells
    (Elsevier Science Bv, 2017) Tengan, Celia H. [UNIFESP]; Moraes, Carlos T.
    Nitric oxide (NO) is a signaling molecule with multiple facets and involved in numerous pathological process, including cancer. Among the different pathways where NO has a functionally relevant participation, is the control of mitochondrial respiration and biogenesis. NO is able to inhibit the electron transport chain, mainly at Complex IV, regulating oxygen consumption and ATP generation, but at the same time, can also induce increase in reactive oxygen and nitrogen species. The presence of reactive species can induce oxidative damage or participate in redox signaling. In this review, we discuss how NO affects mitochondrial respiration and mitochondrial biogenesis, and how it influences the development of mitochondrial deficiency and cancer. This article is part of a Special Issue entitled Mitochondria in Cancer, edited by Giuseppe Gasparre, Rodrigue Rossignol and Pierre Sonveaux. (C) 2017 Elsevier B.V. All rights reserved.