Luisa Rossi
Luisa Rossi
affiliation: Università di Roma Tor Vergata
research area(s): Chemical Biology, Cell Biology
Course: Cell and Molecular Biology
University/Istitution: Università di Roma Tor Vergata
Born in Rome, 24/11/1958. March 1982: Degree in Biological Sciences, University of Rome “La Sapienza”.
1984-2001: Research Assistant, Faculty of Sciences, University of Rome “Tor Vergata”. November 2001: Associate Professor (BIO10, Biochemistry), Faculty of Sciences, University of Rome “Tor Vergata”. Research fields: 1) mechanism of action and physiological role of of the copper enzyme superoxide dismutase; 2) involvement of reactive oxygen species and role of antioxidants in physiopathological conditions (AIDS, cardiac and cerebral ischemia, genetic diseases, tumours); 3) mechanisms of activation and toxicity of xenobiotics and drugs (bipyridils, quinones, nitrofurans) in several cell models; 4) studies on copper metabolism in genetic or experimentally induced alterations of copper homeostasis; study on the involvement of transition metals in the aetiopathogenesis of neurodegenerative diseases.
Copper (Cu) is an essential micronutrient for all organisms because it is a fundamental catalytic and structural cofactor for many enzymes and proteins. On the other hand, when its redox properties are not controlled, it may behave as a noxious pro-oxidant agent. Consequently, organisms have evolved mechanisms strictly regulating intracellular Cu levels; this control is mediated by carrier proteins (“copper chaperones”) surveying the uptake of Cu, its correct insertion in the cupro-enzymes during their synthesis, and the efflux of the metal in excess; at the same time, they impede that free redox active Cu exists intracellularly. All chaperones are characterized by the presence of one or more Cu-binding domains (CXXC), involving redox cysteines.
Particularly, the distribution of Cu to mitochondria to fulfill the activity of the cupro-enzyme cytochrome c oxidase, is a complex mechanism, involving many protein agents, some of them possibly unknown. Furthermore, it has been proposed that copper is stored within the mitochondrial matrix in a still not identified copper-ligand complex. Furthermore, the mitochondrial pool of copper seems to be in a dynamic state, being able to respond to the copper requirement of the cytosol.
The aim of the current research activity is to contribute to the comprehension of the mechanisms underlying the distribution of Cu in the mitochondria, with particular focus on the possible role played by the cellular and mitochondrial redox status.
Arciello M., Rotilio G., Rossi L. (2005) Copper-dependent toxicity in SH-SY5Y neuroblastoma cells involves mitochondrial damage. Biochem. Biophys. Res. Commun. 327: 454-459.

Squitti, R., Barbati, G., Rossi, L., Ventriglia M., Dal Forno G., Cesaretti S., Moffa F., Caridi I., Cassetta E., Pasqualetti P., Calabrese L., Lupoi D., Rossini P.M. (2006) Excess of non-ceruloplasmin serum copper in AD correlates with MMSE, CSF β-amyloid and h-tau. Neurology. 67: 76-82.

Rossi L., Arciello M., Capo C., Rotilio G. (2006) Copper imbalance and oxidative stress in neurodegeneration. Ital. J. Biochem. 55: 212-221.

Rossi L., Squitti R., Calabrese L., Rotilio G., Rossini P. M. (2007) Alteration of peripheral markers of copper homeostasis in Alzheimer’s disease patients: implications in aetiology and therapy. J. Nutr. Health Aging. 11: 408-417.

Dell'Anna M. L., Ottaviani M., Albanesi V., Vidolin A. P., Leone G., Ferraro C., Cossarizza A., Rossi L., Picardo M. (2007) Membrane lipid alterations as a possible basis for melanocyte degeneration in vitiligo. J. Invest. Dermatol. 127: 1226-1233.

Capo, C., Arciello, M., Calabrese, L., Squitti, R., Rossini, P. M., Rossi, L. (2007) Features of ceruloplasmin in the cerebrospinal fluid of Alzheimer’s disease patients. BioMetals, 21, 367-372.

Rossi L., Mazzitelli S., Arciello M., Capo C.R., Rotilio G.(2008) Benefits from diet polyphenols for brain aging and Alzheimer’s disease. Neurochem. Res., 33, 2390-2400.

Arciello M., Capo C. R., Cozzolino M., Ferri A., Nencini M., Carrì M. T., Rossi L. (2010) Inactivation of cytochrome c oxidase by mutant SOD1s in mouse motoneuronal NSC-34 cells is independent from copper availability but is because of nitric oxide. J Neurochem. 112, 183-192.
Arciello M., Capo C. R., Rossi L. Alterations of the homeostasis of the transition metal copper in neurodegenerative disorders. In: Metabolic Influences on Neurological Disorders (Doherty GH ed.), pp. 69-97, 978-81-7895-481-3, Trans World Research Network, Kerala India, 2010.

Avigliano L., Capo C. R., Rossi L. Dietary phytochemicals and drugs: potential consequences of a common metabolism. In: Biochemical Aspects of Human Nutrition (Avigliano L., Rossi L. eds.), pp. 363-382 , Trans World Research Network, Kerala India, 2010. ISBN 978-81-7895-478-3, 2010.

Dell'Anna ML, Ottaviani M, Bellei B, Albanesi V, Cossarizza A, Rossi L. Picardo M. Membrane lipid defects are responsible for the generation of reactive oxygen species in peripheral blood mononuclear cells from vitiligo patients. J Cell Physiol. 223:187-93, 2010.

Arciello M., Capo C. R., D’Annibale, S., Cozzolino, M., Ferri, A., Carrì, MT, Rossi, L. (2011) Copper depletion increases the mitochondrial-associated SOD1 in neuronal cells. BioMetals 24, 269-278.
No projects are available to students for the current accademic year.