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  1. Article ; Online: Mitochondrial Transport in Glycolysis and Gluconeogenesis

    Salvatore Passarella / Avital Schurr / Piero Portincasa

    International Journal of Molecular Sciences, Vol 22, Iss 12620, p

    Achievements and Perspectives

    2021  Volume 12620

    Abstract: Some metabolic pathways involve two different cell components, for instance, cytosol and mitochondria, with metabolites traffic occurring from cytosol to mitochondria and vice versa, as seen in both glycolysis and gluconeogenesis. However, the knowledge ... ...

    Abstract Some metabolic pathways involve two different cell components, for instance, cytosol and mitochondria, with metabolites traffic occurring from cytosol to mitochondria and vice versa, as seen in both glycolysis and gluconeogenesis. However, the knowledge on the role of mitochondrial transport within these two glucose metabolic pathways remains poorly understood, due to controversial information available in published literature. In what follows, we discuss achievements, knowledge gaps, and perspectives on the role of mitochondrial transport in glycolysis and gluconeogenesis. We firstly describe the experimental approaches for quick and easy investigation of mitochondrial transport, with respect to cell metabolic diversity. In addition, we depict the mitochondrial shuttles by which NADH formed in glycolysis is oxidized, the mitochondrial transport of phosphoenolpyruvate in the light of the occurrence of the mitochondrial pyruvate kinase, and the mitochondrial transport and metabolism of L-lactate due to the L-lactate translocators and to the mitochondrial L-lactate dehydrogenase located in the inner mitochondrial compartment.
    Keywords mitochondrial transport ; glycolysis ; gluconeogenesis ; mitochondrial shuttles ; phosphoenolpyruvate ; L-lactate ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 570
    Language English
    Publishing date 2021-11-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Nonalcoholic Fatty Liver Disease (NAFLD). Mitochondria as Players and Targets of Therapies?

    Agostino Di Ciaula / Salvatore Passarella / Harshitha Shanmugam / Marica Noviello / Leonilde Bonfrate / David Q.-H. Wang / Piero Portincasa

    International Journal of Molecular Sciences, Vol 22, Iss 5375, p

    2021  Volume 5375

    Abstract: Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and represents the hepatic expression of several metabolic abnormalities of high epidemiologic relevance. Fat accumulation in the hepatocytes results in cellular fragility ... ...

    Abstract Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and represents the hepatic expression of several metabolic abnormalities of high epidemiologic relevance. Fat accumulation in the hepatocytes results in cellular fragility and risk of progression toward necroinflammation, i.e., nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and eventually hepatocellular carcinoma. Several pathways contribute to fat accumulation and damage in the liver and can also involve the mitochondria, whose functional integrity is essential to maintain liver bioenergetics. In NAFLD/NASH, both structural and functional mitochondrial abnormalities occur and can involve mitochondrial electron transport chain, decreased mitochondrial β-oxidation of free fatty acids, excessive generation of reactive oxygen species, and lipid peroxidation. NASH is a major target of therapy, but there is no established single or combined treatment so far. Notably, translational and clinical studies point to mitochondria as future therapeutic targets in NAFLD since the prevention of mitochondrial damage could improve liver bioenergetics.
    Keywords lipotoxicity ; liver steatosis ; mitochondria ; nitrosative stress ; oxidative stress ; steatohepatitis ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2021-05-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article: The occurrence of l-lactate dehydrogenase in the inner mitochondrial compartment of pig liver

    Paventi, Gianluca / Roberto Pizzuto / Salvatore Passarella

    Biochemical and biophysical research communications. 2017 July 22, v. 489

    2017  

    Abstract: Although pig represents a model species in biomedical research including studies dealing with liver patho-physiology, some aspects of liver metabolism need to be addressed. In particular, whether and how pig mitochondria can metabolize l-lactate remains ... ...

    Abstract Although pig represents a model species in biomedical research including studies dealing with liver patho-physiology, some aspects of liver metabolism need to be addressed. In particular, whether and how pig mitochondria can metabolize l-lactate remains to be established. We show here that pig liver mitochondria (PLM) possess their own l-lactate dehydrogenase (mL-LDH). This was shown both via immunological analysis and by assaying photometrically the L-LDH reaction in solubilised PLM. The mL-LDH reaction shows hyperbolic dependence on the substrate concentration, it is inhibited by oxamate and proves to differ from the cytosolic activity (cL-LDH), as revealed by the difference found in both pH profiles and temperature dependence of m- and cL-LDH. Titration experiments with digitonin show that mL-LDH is restricted in mitochondrial inner compartment. In agreement with the above findings, three genes in Sus scrofa genome encoded for L-LDH subunits which are predicted to have mitochondrial localization, as investigated by Target P 1.1 and PredSL analysis.
    Keywords Sus scrofa ; biomedical research ; digitonin ; genes ; lactic acid ; liver ; metabolism ; mitochondria ; models ; pH ; solubilization ; swine ; temperature ; titration
    Language English
    Dates of publication 2017-0722
    Size p. 255-261.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2017.05.154
    Database NAL-Catalogue (AGRICOLA)

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  4. Article ; Online: The role of mitochondria in yeast programmed cell death

    SergioGiannattasio / SalvatorePassarella

    Frontiers in Oncology, Vol

    2012  Volume 2

    Abstract: Mammalian apoptosis and yeast programmed cell death (PCD) share a variety of features including ROS production, protease activity and a major role played by mitochondria. In view of this, and of the distinctive characteristics differentiating yeast and ... ...

    Abstract Mammalian apoptosis and yeast programmed cell death (PCD) share a variety of features including ROS production, protease activity and a major role played by mitochondria. In view of this, and of the distinctive characteristics differentiating yeast and multicellular organism PCD, the mitochondrial contribution to cell death in the genetically tractable yeast Saccharomyces cerevisiae has been intensively investigated. In this mini-review we report whether and how yeast mitochondrial function and proteins belonging to oxidative phosphorylation, protein trafficking into and out of mitochondria, and mitochondrial dynamics, play a role in PCD. Since in PCD many processes take place over time, emphasis will be placed on an experimental model based on acetic acid induced PCD (AA-PCD) which has the unique feature of having been investigated as a function of time. As will be described there are at least two AA-PCD pathways each with a multifaceted role played by mitochondrial components, in particular by cytochrome c.
    Keywords Acetic Acid ; Mitochondria ; Protein trafficking ; yeast ; programmed cell death ; intracellular signalling ; cytochrome c ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R
    Subject code 570
    Language English
    Publishing date 2012-07-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article: Prostate cancer cells metabolize d-lactate inside mitochondria via a d-lactate dehydrogenase which is more active and highly expressed than in normal cells

    de Bari, Lidia / Loredana Moro / Salvatore Passarella

    Federation of European Biochemical Societies FEBS letters. 2013 Mar. 01, v. 587, no. 5

    2013  

    Abstract: Although d-lactate metabolism has been shown to occur in a variety of mitochondria, the metabolic fate of d-lactate in cancer cells has never been investigated, as it is believed to be exported to the extracellular phase. We show that mitochondria from ... ...

    Abstract Although d-lactate metabolism has been shown to occur in a variety of mitochondria, the metabolic fate of d-lactate in cancer cells has never been investigated, as it is believed to be exported to the extracellular phase. We show that mitochondria from both cancer (PC-3) and normal (PNT1A) prostate cells can metabolize d-lactate in an energy competent manner. This is due to the mitochondrial d-lactate dehydrogenase, a membrane flavoprotein, the activity and protein level of which are higher in PC-3 than in PNT1A cells, as detected by both kinetic and immunological analysis. d-Lactate can enter prostate mitochondria and cause the export of newly synthesized malate in a carrier-mediated manner, with the rate of malate efflux from mitochondria twofold higher in cancer.
    Keywords energy ; flavoproteins ; malates ; metabolism ; mitochondria ; neoplasm cells ; prostatic neoplasms
    Language English
    Dates of publication 2013-0301
    Size p. 467-473.
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2013.01.011
    Database NAL-Catalogue (AGRICOLA)

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