Affiliation: University of Bologna
- Evaluating mitochondrial membrane potential in cellsGiancarlo Solaini
Dipartimento di Biochimica, Universita di Bologna, Via Irnerio 48, Bologna, 40126, Italy
Biosci Rep 27:11-21. 2007..Furthermore, we discuss the application and feasibility of various techniques and discuss their respective strength and weakness...
- Oxidative phosphorylation in cancer cellsGiancarlo Solaini
Department of Biochemistry G Moruzzi, University of Bologna, Via Irnerio 48, 40126 Bologna, Italy
Biochim Biophys Acta 1807:534-42. 2011..Here, we review the peculiarity of tumour mitochondrial bioenergetics and the mode it is linked to the cell metabolism, providing a short overview of the evidence accumulated so far, but highlighting the more recent advances...
- Hypoxia and mitochondrial oxidative metabolismGiancarlo Solaini
Department of Biochemistry G Moruzzi, University of Bologna, Bologna, Italy
Biochim Biophys Acta 1797:1171-7. 2010..In addition, we address the involvement of HIF-1 and the inhibitor protein of F1F0 ATPase in the hypoxia-induced mitochondrial autophagy...
- The study of the pathogenic mechanism of mitochondrial diseases provides information on basic bioenergeticsGiancarlo Solaini
Dipartimento di Biochimica G Moruzzi, Via Irnerio, 48, Universita di Bologna, Italy
Biochim Biophys Acta 1777:941-5. 2008..We propose that the integrity of transmembrane helix III is essential for the mechanical function of ATPase 6 as a stator element in the ATP synthase, but that it is not relevant for oligomycin inhibition...
- Biochemical phenotypes associated with the mitochondrial ATP6 gene mutations at nt8993Alessandra Baracca
Dipartimento di Biochimica G Moruzzi, Via Irnerio 48, Universita di Bologna, 40126 Bologna, and Fondazione Ospedale Maggiore IRCCS Centro Dino Ferrari, Milano, Italy
Biochim Biophys Acta 1767:913-9. 2007....
- Human NARP mitochondrial mutation metabolism corrected with alpha-ketoglutarate/aspartate: a potential new therapyGianluca Sgarbi
Dipartimento di Biochimica G Moruzzi, Universita di Bologna, Bologna, Italy
Arch Neurol 66:951-7. 2009....
- Mitochondrial Complex I decrease is responsible for bioenergetic dysfunction in K-ras transformed cellsAlessandra Baracca
Department of Biochemistry G Moruzzi, University of Bologna, Bologna, Italy
Biochim Biophys Acta 1797:314-23. 2010..Taken together, our results provide the new insight that the reduction of respiration observed in K-ras transformed cells is specifically due to a Complex I activity decrease...
- Mitochondrial respiratory chain super-complex I-III in physiology and pathologyGiorgio Lenaz
Dipartimento di Biochimica, Universita di Bologna, Via Irnerio 48, 40126 Bologna, Italy
Biochim Biophys Acta 1797:633-40. 2010..There is increasing evidence that disruption of the super-complex organization leads to functional derangements responsible for pathological changes, as we have found in K-ras-transformed fibroblasts...
- Bioenergetics of mitochondrial diseases associated with mtDNA mutationsGiorgio Lenaz
Dipartimento di Biochimica G Moruzzi, Universita di Bologna, Via Irnerio 48, Bologna 40126, Italy
Biochim Biophys Acta 1658:89-94. 2004....
- Severe impairment of complex I-driven adenosine triphosphate synthesis in leber hereditary optic neuropathy cybridsAlessandra Baracca
Dipartimento di Biochimica, University of Bologna, Italy
Arch Neurol 62:730-6. 2005..Leber hereditary optic neuropathy (LHON) is a maternally inherited form of central vision loss associated with mitochondrial DNA point mutations that affect the ND subunits of complex I...
- Glucose plays a main role in human fibroblasts adaptation to hypoxiaAlessandra Baracca
Dipartimento di Scienze Biomediche e Neuromotorie, Universita di Bologna, Via Irnerio 48, 40126 Bologna, Italy
Int J Biochem Cell Biol 45:1356-65. 2013..Therefore, our data show for the first time that glucose availability significantly affects the hypoxia-induced HIF-1/BNIP3 response, and in particular glucose absence results in enhancing the OXPHOS rate...
- Inefficient coupling between proton transport and ATP synthesis may be the pathogenic mechanism for NARP and Leigh syndrome resulting from the T8993G mutation in mtDNAGianluca Sgarbi
Dipartimento di Biochimica G Moruzzi, Via Irnerio 48, Universita di Bologna, 40126 Bologna, Italy
Biochem J 395:493-500. 2006..We discuss our findings in view of the current knowledge regarding the rotary mechanism of catalysis of the enzyme...
- Bioenergetics shapes cellular death pathways in Leber's hereditary optic neuropathy: a model of mitochondrial neurodegenerationValerio Carelli
Dipartimento di Scienze Neurologiche, Universita di Bologna, Via Ugo Foscolo 7, 40123 Bologna, Italy
Biochim Biophys Acta 1658:172-9. 2004....
- New insights into structure and function of mitochondria and their role in aging and diseaseGiorgio Lenaz
Dipartimento di Biochimica, Universita di Bologna, Bologna, Italy
Antioxid Redox Signal 8:417-37. 2006..Evidence is presented favoring the mitochondrial theory, with primary mitochondrial alterations, although the problem is made more complex by changes in the cross-talk between nuclear and mitochondrial DNA...
- Rhodamine 123 as a probe of mitochondrial membrane potential: evaluation of proton flux through F(0) during ATP synthesisAlessandra Baracca
Department of Biochemistry G Moruzzi Alma Mater Studiorum University of Bologna, Via Irnerio 48, I 40126, Bologna, Italy
Biochim Biophys Acta 1606:137-46. 2003....
- Mitochondrial Complex I: structure, function, and implications in neurodegenerationGiorgio Lenaz
Dipartimento di Biochimica G Moruzzi, Universita di Bologna, Italy
Ital J Biochem 55:232-53. 2006....
- Fluorescence resonance energy transfer between coumarin-derived mitochondrial F(1)-ATPase gamma subunit and pyrenylmaleimide-labelled fragments of IF(1) and c subunitAlessandra Baracca
Dipartimento di Biochimica G Moruzzi, Universita degli Studi di Bologna, Via Irnerio 48, 40126 Bologna, Italy
Biochem J 362:165-71. 2002....
- Biochemical-clinical correlation in patients with different loads of the mitochondrial DNA T8993G mutationValerio Carelli
Istituto di Clinica Neurologica, Universita di Bologna, Via U Foscolo 7, 40123 Bologna, Italy
Arch Neurol 59:264-70. 2002....
- The inhibitor protein (IF1) of the F1F0-ATPase modulates human osteosarcoma cell bioenergeticsSimona Barbato
From the Department of Biomedical and NeuroMotor Sciences DIBINEM, University of Bologna, Via Irnerio 48, 40126 Bologna, Italy
J Biol Chem 290:6338-48. 2015....
- Hyperoxia fully protects mitochondria of explanted liversG Sgarbi
Department of Biochemistry, University of Bologna, Via Irnerio, 48, 40126, Bologna, Italy
J Bioenerg Biomembr 43:673-82. 2011..Remarkably, liver perfusion with hyperoxic solutions fully preserved mitochondrial morphology and function, suggesting that perfusion of the graft with hyperoxic solution should be considered in human transplantation...
- Biochemical analysis of respiratory function in cybrid cell lines harbouring mitochondrial DNA mutationsFrancesco Pallotti
Department of Neurology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA
Biochem J 384:287-93. 2004..However, the distinct clinical features associated with some of these mutations still remain to be elucidated...
- Decreased platelet cytochrome c oxidase activity is accompanied by increased blood lactate concentration during exercise in patients with Alzheimer diseaseMichelangelo Mancuso
Department of Neurosciences, Neurological Clinics, University of Pisa, Via Roma 67, 56126, Pisa, Italy
Exp Neurol 182:421-6. 2003..These results support the hypothesis of a systemic impairment of the mitochondrial function in AD and indicate that decreased COX activity could have functional consequences on metabolism...
- Cytochrome c oxidase and mitochondrial F1F0-ATPase (ATP synthase) activities in platelets and brain from patients with Alzheimer's diseaseFrancesca Bosetti
Scuola Superiore di Studi Universitari e di Perfezionamento S Anna, Via G Carducci 40, 56127 Pisa, Italy
Neurobiol Aging 23:371-6. 2002..A reduced COX activity may make the tissue vulnerable to excitotoxicity or reduced oxygen availability...
- Severe ultrastructural mitochondrial changes in lymphoblasts homozygous for Huntington disease mutationFerdinando Squitieri
Neurogenetics Unit, IRCCS Neuromed, Pozzilli, IS, Italy
Mech Ageing Dev 127:217-20. 2006..We argue that early mitochondrial impairment at basal level may affect the severity of HD progression in patients...
- Guanidine-induced dissociation of mitochondrial F1-ATPaseStavros Papageorgiou
Scuola Superiore di Studi Universitari e di Perfezionamento S Anna, Piazza dei Martiri della Libertà, 33, 56127 Pisa, Italy
Ital J Biochem 53:148-56. 2004..Our results suggest that the delta and epsilon subunits are loosely bound to alpha3beta3gamma , and play an important role in determining structural stability to isolated mitochondrial F1-ATPase...
- Quenching of intracellular ROS generation as a mechanism for oleate-induced reduction of endothelial activation and early atherogenesisMarika Massaro
Laboratory for Thrombosis and Vascular Research, C N R Institute of Clinical Physiology, Pisa, Italy
Thromb Haemost 88:335-44. 2002..These results indicate that oleate may exert direct vascular atheroprotective effects by inhibiting endothelial activation through a quenching of stimuli-induced increase in ROS...