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Article ; Online: Functional Foods: An Approach to Modulate Molecular Mechanisms of Alzheimer's Disease.

Atlante, Anna / Amadoro, Giuseppina / Bobba, Antonella / Latina, Valentina

2020 Volume 9, Issue 11

Abstract: A new epoch is emerging with intense research on nutraceuticals, i.e., "food or food product that provides medical or health benefits including the prevention and treatment of diseases", such as Alzheimer's disease. Nutraceuticals act at different ... ...

Abstract	A new epoch is emerging with intense research on nutraceuticals, i.e., "food or food product that provides medical or health benefits including the prevention and treatment of diseases", such as Alzheimer's disease. Nutraceuticals act at different biochemical and metabolic levels and much evidence shows their neuroprotective effects; in particular, they are able to provide protection against mitochondrial damage, oxidative stress, toxicity of β-amyloid and Tau and cell death. They have been shown to influence the composition of the intestinal microbiota significantly contributing to the discovery that differential microorganisms composition is associated with the formation and aggregation of cerebral toxic proteins. Further, the routes of interaction between epigenetic mechanisms and the microbiota-gut-brain axis have been elucidated, thus establishing a modulatory role of diet-induced epigenetic changes of gut microbiota in shaping the brain. This review examines recent scientific literature addressing the beneficial effects of some natural products for which mechanistic evidence to prevent or slowdown AD are available. Even if the road is still long, the results are already exceptional.
MeSH term(s)	Alzheimer Disease/etiology ; Alzheimer Disease/metabolism ; Alzheimer Disease/therapy ; Amyloid beta-Peptides/metabolism ; Animals ; Biological Products/pharmacology ; Biomarkers ; Brain/drug effects ; Brain/metabolism ; Brain/pathology ; DNA Methylation ; Diet Therapy ; Dietary Supplements ; Disease Management ; Disease Susceptibility ; Functional Food ; Gastrointestinal Microbiome/drug effects ; Gene Expression Regulation/drug effects ; Humans ; Mitochondria/drug effects ; Mitochondria/genetics ; Mitochondria/metabolism ; Neuroprotective Agents/pharmacology
Chemical Substances	Amyloid beta-Peptides ; Biological Products ; Biomarkers ; Neuroprotective Agents
Language	English
Publishing date	2020-10-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9112347
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: An Intriguing Involvement of Mitochondria in Cystic Fibrosis.

Favia, Maria / de Bari, Lidia / Bobba, Antonella / Atlante, Anna

Journal of clinical medicine

2019 Volume 8, Issue 11

Abstract: Cystic fibrosis (CF) occurs when the cystic fibrosis transmembrane conductance regulator (CFTR) protein is not synthetized and folded correctly. The CFTR protein helps to maintain the balance of salt and water on many body surfaces, such as the lung ... ...

Abstract	Cystic fibrosis (CF) occurs when the cystic fibrosis transmembrane conductance regulator (CFTR) protein is not synthetized and folded correctly. The CFTR protein helps to maintain the balance of salt and water on many body surfaces, such as the lung surface. When the protein is not working correctly, chloride becomes trapped in cells, then water cannot hydrate the cellular surface and the mucus covering the cells becomes thick and sticky. Furthermore, a defective CFTR appears to produce a redox imbalance in epithelial cells and extracellular fluids and to cause an abnormal generation of reactive oxygen species: as a consequence, oxidative stress has been implicated as a causative factor in the aetiology of the process. Moreover, massive evidences show that defective CFTR gives rise to extracellular GSH level decrease and elevated glucose concentrations in airway surface liquid (ASL), thus encouraging lung infection by pathogens in the CF advancement. Recent research in progress aims to rediscover a possible role of mitochondria in CF. Here the latest new and recent studies on mitochondrial bioenergetics are collected. Surprisingly, they have enabled us to ascertain that mitochondria have a leading role in opposing the high ASL glucose level as well as oxidative stress in CF.
Language	English
Publishing date	2019-11-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm8111890
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Article: RTG Signaling Sustains Mitochondrial Respiratory Capacity in HOG1-Dependent Osmoadaptation

Guaragnella, Nicoletta / Agrimi, Gennaro / Scarcia, Pasquale / Suriano, Clelia / Pisano, Isabella / Bobba, Antonella / Mazzoni, Cristina / Palmieri, Luigi / Giannattasio, Sergio

Microorganisms. 2021 Sept. 06, v. 9, no. 9

2021

Abstract: Mitochondrial RTG-dependent retrograde signaling, whose regulators have been characterized in Saccharomyces cerevisiae, plays a recognized role under various environmental stresses. Of special significance, the activity of the transcriptional complex ... ...

Abstract	Mitochondrial RTG-dependent retrograde signaling, whose regulators have been characterized in Saccharomyces cerevisiae, plays a recognized role under various environmental stresses. Of special significance, the activity of the transcriptional complex Rtg1/3 has been shown to be modulated by Hog1, the master regulator of the high osmolarity glycerol pathway, in response to osmotic stress. The present work focuses on the role of RTG signaling in salt-induced osmotic stress and its interaction with HOG1. Wild-type and mutant cells, lacking HOG1 and/or RTG genes, are compared with respect to cell growth features, retrograde signaling activation and mitochondrial function in the presence and in the absence of high osmostress. We show that RTG2, the main upstream regulator of the RTG pathway, contributes to osmoadaptation in an HOG1-dependent manner and that, with RTG3, it is notably involved in a late phase of growth. Our data demonstrate that impairment of RTG signaling causes a decrease in mitochondrial respiratory capacity exclusively under osmostress. Overall, these results suggest that HOG1 and the RTG pathway may interact sequentially in the stress signaling cascade and that the RTG pathway may play a role in inter-organellar metabolic communication for osmoadaptation.
Keywords	Saccharomyces cerevisiae ; cell growth ; glycerol ; mitochondria ; mutants ; osmolarity ; osmotic stress ; osmotolerance ; transcription (genetics)
Language	English
Dates of publication	2021-0906
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms9091894
Database	NAL-Catalogue (AGRICOLA)

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Article: RTG

Guaragnella, Nicoletta / Agrimi, Gennaro / Scarcia, Pasquale / Suriano, Clelia / Pisano, Isabella / Bobba, Antonella / Mazzoni, Cristina / Palmieri, Luigi / Giannattasio, Sergio

Microorganisms

2021 Volume 9, Issue 9

Abstract: ... ...

Abstract	Mitochondrial
Language	English
Publishing date	2021-09-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms9091894
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Article ; Online: A disease with a sweet tooth: exploring the Warburg effect in Alzheimer's disease.

Atlante, Anna / de Bari, Lidia / Bobba, Antonella / Amadoro, Giuseppina

Biogerontology

2017 Volume 18, Issue 3, Page(s) 301–319

Abstract: After more than 80 years from the revolutionary discoveries of Otto Warburg, who observed high glucose dependency, with increased glycolysis and lactate production regardless of oxygen availability in most cancer cells, the 'Warburg effect' returns to ... ...

Abstract	After more than 80 years from the revolutionary discoveries of Otto Warburg, who observed high glucose dependency, with increased glycolysis and lactate production regardless of oxygen availability in most cancer cells, the 'Warburg effect' returns to the fore in neuronal cells affected by Alzheimer's disease (AD). Indeed, it seems that, in the mild phase of AD, neuronal cells "prefer" to use the energetically inefficient method of burning glucose by glycolysis, as in cancer, proving to become resistant to β-amyloid (Aβ)-dependent apoptosis. However, in the late phase, while most AD brain cells die in response to Aβ toxicity, only small populations of neurons, exhibiting increased glucose uptake and glycolytic flux, are able to survive as they are resistant to Aβ. Here we draw an overview on the metabolic shift for glucose utilization from oxidative phosphorylation to glycolysis, focusing on the hypothesis that, as extreme attempt to oppose the impending death, mitochondria-whose dysfunction and central role in Aβ toxicity is an AD hallmark-are sent into quiescence, this likely contributing to activate mechanisms of resistance to Aβ-dependent apoptosis. Finally, the attempt turns out fruitless since the loss of the adaptive advantage afforded by elevated aerobic glycolysis exacerbates the pathophysiological processes associated with AD, making the brain susceptible to Aβ-induced neurotoxicity and leading to cell death and dementia. The understanding of how certain nerve cells become resistant to Aβ toxicity, while the majority dies, is an attractive challenge toward the identification of novel possible targets for AD therapy.
Language	English
Publishing date	2017-06
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2047160-9
ISSN	1573-6768 ; 1389-5729
ISSN (online)	1573-6768
ISSN	1389-5729
DOI	10.1007/s10522-017-9692-x
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Article: Yeast as a Model to Unravel New BRCA2 Functions in Cell Metabolism.

Costanza, Alessandra / Guaragnella, Nicoletta / Bobba, Antonella / Manzari, Caterina / L'Abbate, Alberto / Giudice, Claudio Lo / Picardi, Ernesto / D'Erchia, Anna Maria / Pesole, Graziano / Giannattasio, Sergio

Frontiers in oncology

2022 Volume 12, Page(s) 908442

Abstract: Mutations in BRCA2 gene increase the risk for breast cancer and for other cancer types, including pancreatic and prostate cancer. Since its first identification as an oncosupressor in 1995, the best-characterized function of BRCA2 is in the repair of DNA ...

Abstract	Mutations in BRCA2 gene increase the risk for breast cancer and for other cancer types, including pancreatic and prostate cancer. Since its first identification as an oncosupressor in 1995, the best-characterized function of BRCA2 is in the repair of DNA double-strand breaks (DSBs) by homologous recombination. BRCA2 directly interacts with both RAD51 and single-stranded DNA, mediating loading of RAD51 recombinase to sites of single-stranded DNA. In the absence of an efficient homologous recombination pathway, DSBs accumulate resulting in genome instability, thus supporting tumorigenesis. Yet the precise mechanism by which BRCA2 exerts its tumor suppressor function remains unclear. BRCA2 has also been involved in other biological functions including protection of telomere integrity and stalled replication forks, cell cycle progression, transcriptional control and mitophagy. Recently, we and others have reported a role of BRCA2 in modulating cell death programs through a molecular mechanism conserved in yeast and mammals. Here we hypothesize that BRCA2 is a multifunctional protein which exerts specific functions depending on cell stress response pathway. Based on a differential RNA sequencing analysis carried out on yeast cells either growing or undergoing a regulated cell death process, either in the absence or in the presence of BRCA2, we suggest that BRCA2 causes central carbon metabolism reprogramming in response to death stimuli and encourage further investigation on the role of metabolic reprogramming in BRCA2 oncosuppressive function.
Language	English
Publishing date	2022-06-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2022.908442
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Article ; Online: Characterization of mitochondrial function in cells with impaired cystic fibrosis transmembrane conductance regulator (CFTR) function.

Atlante, Anna / Favia, Maria / Bobba, Antonella / Guerra, Lorenzo / Casavola, Valeria / Reshkin, Stephan Joel

Journal of bioenergetics and biomembranes

2016 Volume 48, Issue 3, Page(s) 197–210

Abstract: Evidence supporting the occurrence of oxidative stress in Cystic Fibrosis (CF) is well established and the literature suggests that oxidative stress is inseparably linked to mitochondrial dysfunction. Here, we have characterized mitochondrial function, ... ...

Abstract	Evidence supporting the occurrence of oxidative stress in Cystic Fibrosis (CF) is well established and the literature suggests that oxidative stress is inseparably linked to mitochondrial dysfunction. Here, we have characterized mitochondrial function, in particular as it regards the steps of oxidative phosphorylation and ROS production, in airway cells either homozygous for the F508del-CFTR allele or stably expressing wt-CFTR. We find that oxygen consumption, ΔΨ generation, adenine nucleotide translocator-dependent ADP/ATP exchange and both mitochondrial Complex I and IV activities are impaired in CF cells, while both mitochondrial ROS production and membrane lipid peroxidation increase. Importantly, treatment of CF cells with the small molecules VX-809 and 4,6,4'-trimethylangelicin, which act as "correctors" for F508del CFTR by rescuing the F508del CFTR-dependent chloride secretion, while having no effect per sè on mitochondrial function in wt-CFTR cells, significantly improved all the above mitochondrial parameters towards values found in the airway cells expressing wt-CFTR. This novel study on mitochondrial bioenergetics provides a springboard for future research to further understand the molecular mechanisms responsible for the involvement of mitochondria in CF and identify the proteins primarily responsible for the F508del-CFTR-dependent mitochondrial impairment and thus reveal potential novel targets for CF therapy.
MeSH term(s)	Aminopyridines/pharmacology ; Aminopyridines/therapeutic use ; Benzodioxoles/pharmacology ; Benzodioxoles/therapeutic use ; Cells, Cultured ; Chlorides/metabolism ; Cystic Fibrosis/drug therapy ; Cystic Fibrosis/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator/physiology ; Energy Metabolism/drug effects ; Energy Metabolism/genetics ; Furocoumarins/pharmacology ; Furocoumarins/therapeutic use ; Humans ; Mitochondrial Diseases/drug therapy ; Mitochondrial Diseases/metabolism ; Mitochondrial Diseases/physiopathology ; Mutation ; Respiratory System/cytology
Chemical Substances	Aminopyridines ; Benzodioxoles ; Chlorides ; Furocoumarins ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; lumacaftor (EGP8L81APK) ; 4,4',6-trimethylangelicin (T2MYR3390L)
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	198499-8
ISSN	1573-6881 ; 0145-479X ; 0449-5705
ISSN (online)	1573-6881
ISSN	0145-479X ; 0449-5705
DOI	10.1007/s10863-016-9663-y
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Article ; Online: Antioxidant role of hydroxytyrosol on oxidative stress in cadmium-intoxicated rats: different effect in spleen and testes.

Merra, Elisabetta / Calzaretti, Giovanna / Bobba, Antonella / Storelli, Maria M / Casalino, Elisabetta

Drug and chemical toxicology

2014 Volume 37, Issue 4, Page(s) 420–426

Abstract: Hydroxytyrosol (2-(3,4dihydroxyphenyl)ethanol, (DPE), a phenolic compound present in olive oil, is known to have antioxidant properties. The aim of this study was to investigate the effect of DPE on oxidative stress induced by cadmium injections (CdCl2 2. ...

Abstract	Hydroxytyrosol (2-(3,4dihydroxyphenyl)ethanol, (DPE), a phenolic compound present in olive oil, is known to have antioxidant properties. The aim of this study was to investigate the effect of DPE on oxidative stress induced by cadmium injections (CdCl2 2.5 mg/kg body weight) in spleen and testes of adult male rats. Oxidative stress was evaluated by measuring lipid peroxidation by thiobarbituric acid reactive substances (TBARS) as well as superoxide dismutase (SOD) and catalase (CAT) activities in cytosol and mitochondria. We found that in spleen no TBARS formation was detected following CdCl2 injections; however, DPE induces decrease in TBARS level in treated and untreated rats. On the contrary, we observed that DPE showed no effect on cadmium-induced lipid peroxidation in testes. Cytosolic activities of SOD and CAT decreased significantly only in spleen, where DPE restores the values to the control levels. Noteworthy, mitochondrial activities of SOD and CAT were strongly reduced by cadmium treatment both in spleen and testes, and DPE was not be able to restore their activity. Overall, the results from this study indicated that the DPE has different antioxidant efficiency in spleen and testis of cadmium intoxicated rats.
MeSH term(s)	Animals ; Antioxidants/pharmacology ; Cadmium Chloride/toxicity ; Catalase/metabolism ; Cytosol/drug effects ; Cytosol/metabolism ; Lipid Peroxidation/drug effects ; Male ; Mitochondria/drug effects ; Mitochondria/metabolism ; Oxidative Stress/drug effects ; Phenylethyl Alcohol/analogs & derivatives ; Phenylethyl Alcohol/pharmacology ; Rats ; Rats, Wistar ; Spleen/drug effects ; Spleen/pathology ; Superoxide Dismutase/metabolism ; Testis/drug effects ; Testis/pathology ; Thiobarbituric Acid Reactive Substances/metabolism
Chemical Substances	Antioxidants ; Thiobarbituric Acid Reactive Substances ; 3,4-dihydroxyphenylethanol (10597-60-1) ; Catalase (EC 1.11.1.6) ; Superoxide Dismutase (EC 1.15.1.1) ; Cadmium Chloride (J6K4F9V3BA) ; Phenylethyl Alcohol (ML9LGA7468)
Language	English
Publishing date	2014-01-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	548368-2
ISSN	1525-6014 ; 0148-0545
ISSN (online)	1525-6014
ISSN	0148-0545
DOI	10.3109/01480545.2013.878950
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Article ; Online: Alzheimer's proteins, oxidative stress, and mitochondrial dysfunction interplay in a neuronal model of Alzheimer's disease.

Bobba, Antonella / Petragallo, Vito A / Marra, Ersilia / Atlante, Anna

International journal of Alzheimer's disease

2010 Volume 2010

Abstract: In this paper, we discuss the interplay between beta-amyloid (Aβ) peptide, Tau fragments, oxidative stress, and mitochondria in the neuronal model of cerebellar granule neurons (CGNs) in which the molecular events reminiscent of AD are activated. The ... ...

Abstract	In this paper, we discuss the interplay between beta-amyloid (Aβ) peptide, Tau fragments, oxidative stress, and mitochondria in the neuronal model of cerebellar granule neurons (CGNs) in which the molecular events reminiscent of AD are activated. The identification of the death route and the cause/effect relationships between the events leading to death could be helpful to manage the progression of apoptosis in neurodegeneration and to define antiapoptotic treatments acting on precocious steps of the death process. Mitochondrial dysfunction is among the earliest events linked to AD and might play a causative role in disease onset and progression. Recent studies on CGNs have shown that adenine nucleotide translocator (ANT) impairment, due to interaction with toxic N-ter Tau fragment, contributes in a significant manner to bioenergetic failure and mitochondrial dysfunction. These findings open a window for new therapeutic strategies aimed at preserving and/or improving mitochondrial function.
Language	English
Publishing date	2010-09-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	2573333-3
ISSN	2090-0252 ; 2090-8024
ISSN (online)	2090-0252
ISSN	2090-8024
DOI	10.4061/2010/621870
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Article ; Online: Yeast acetic acid-induced programmed cell death can occur without cytochrome c release which requires metacaspase YCA1.

Guaragnella, Nicoletta / Bobba, Antonella / Passarella, Salvatore / Marra, Ersilia / Giannattasio, Sergio

FEBS letters

2010 Volume 584, Issue 1, Page(s) 224–228

Abstract: To investigate the role of cytochrome c (cyt c) release in yeast acetic acid-induced programmed cell death (AA-PCD), wild type (wt) and cells lacking metacaspase (Deltayca1), cytochrome c (Deltacyc1,7) and both (Deltacyc1,7Deltayca1) were compared for AA- ...

Abstract	To investigate the role of cytochrome c (cyt c) release in yeast acetic acid-induced programmed cell death (AA-PCD), wild type (wt) and cells lacking metacaspase (Deltayca1), cytochrome c (Deltacyc1,7) and both (Deltacyc1,7Deltayca1) were compared for AA-PCD occurrence, hydrogen peroxide (H(2)O(2)) production and caspase activity. AA-PCD occurs in Deltacyc1,7 and Deltacyc1,7Deltayca1 cells slower than in wt, but similar to that in Deltayca1 cells, in which no cytochrome c release occurs. Both H(2)O(2) production and caspase activation occur in these cells with early and extra-activation in Deltacyc1,7 cells. We conclude that alternative death pathways can be activated in yeast AA-PCD, one dependent on cyt c release, which requires YCA1, and the other(s) independent on it.
MeSH term(s)	Acetic Acid/pharmacology ; Apoptosis ; Caspases/genetics ; Caspases/metabolism ; Cytochromes c/genetics ; Cytochromes c/metabolism ; Hydrogen Peroxide/metabolism ; Saccharomyces cerevisiae/drug effects ; Saccharomyces cerevisiae/enzymology ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism
Chemical Substances	Saccharomyces cerevisiae Proteins ; Cytochromes c (9007-43-6) ; Hydrogen Peroxide (BBX060AN9V) ; Caspases (EC 3.4.22.-) ; MCA1 protein, S cerevisiae (EC 3.4.22.-) ; Acetic Acid (Q40Q9N063P)
Language	English
Publishing date	2010-01-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2009.11.072
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