A5070361761- Mitochondrial Function and Pathology
- Cardiac Ischemia and Reperfusion
- Muscle Physiology and Disorders
- Immune cells in cancer
- Adipose Tissue and Metabolism
- Redox biology and oxidative stress
- Photodynamic Therapy Research Studies
- Cardiovascular Effects of Exercise
- Muscle metabolism and nutrition
- Cardiomyopathy and Myosin Studies
- ATP Synthase and ATPases Research
- Coenzyme Q10 studies and effects
- Antibiotics Pharmacokinetics and Efficacy
- Cardiovascular Function and Risk Factors
- Photosynthetic Processes and Mechanisms
- Metabolism and Genetic Disorders
- Photoreceptor and optogenetics research
- Nitric Oxide and Endothelin Effects
- Tissue Engineering and Regenerative Medicine
- Advanced MRI Techniques and Applications
- Vitamin C and Antioxidants Research
- Mast cells and histamine
- Plant chemical constituents analysis
- Infant Nutrition and Health
- Boron Compounds in Chemistry
University of Padua
2015-2024
Città della Speranza Foundation
2018-2024
University of Perugia
2019
Veneto Institute of Molecular Medicine
2017-2018
Medical University of Graz
2012
Leiden University Medical Center
2012
Institute of Cardiology
2012
Sanjay Gandhi Post Graduate Institute of Medical Sciences
2012
University College London
2012
Charles University
2012
The opening of the mitochondrial permeability transition pore (PTP) has been suggested to play a key role in various forms cell death, but direct evidence intact tissues is still lacking. We found that rat heart, 92% NAD+glycohydrolase activity associated with mitochondria. This was not modified by addition Triton X-100, although it abolished mild treatment protease Nagarse, condition did affect energy-linked properties Ca2+ isolated heart mitochondria resulted profound decrease their NAD+...
Although the contribution of reactive oxygen species to myocardial ischemia is well recognized, possible intracellular targets, especially at level myofibrillar proteins (MP), are not yet fully characterized. To assess maximal extent oxidative degradation proteins, isolated rat hearts were perfused with 1 mM H(2)O(2). Subsequently, MP maximally damage was compared effects produced by 1) 30 min no-flow (I) followed in other 3 reperfusion (I/R); and 2) I/R presence a potent antioxidant...
Aims We addressed a potential mechanism of myocardial dysfunction following coronary microembolization at the level myofibrillar proteins.
Several studies documented the key role of oxidative stress and abnormal production reactive oxygen species (ROS) in pathophysiology muscular dystrophies (MDs). The sources ROS, however, are still controversial as well their major molecular targets. This study investigated whether ROS produced mitochondria by monoamine oxidase (MAO) contributes to MD pathogenesis. Pargyline, an MAO inhibitor, reduced accumulation along with a beneficial effect on dystrophic phenotype Col6a1(-/-) mice, model...
The formation of reactive oxygen species (ROS) is increased in heart failure (HF). However, the causal and mechanistic relationship ROS with contractile dysfunction not clear detail. Therefore, formation, myofibrillar protein oxidation p38 MAP kinase activation were related to function failing rabbit hearts.Three weeks rapid left ventricular (LV) pacing reduced LV shortening fraction (SF, echocardiography) from 32 +/- 1% 13 1%. as assessed by dihydroethidine staining, 36 8% was associated...
Abstract Macrophages are essential players for the host response against pathogens, regulation of inflammation and tissue regeneration. The wide range macrophage functions rely on their heterogeneity plasticity that enable a dynamic adaptation responses according to surrounding environmental cues. Recent studies suggest metabolism provides synergistic support activation elicitation desirable immune responses; however, metabolic pathways orchestrating still under scrutiny. Optic atrophy 1...
The complexes formed by partially folded human and bovine α‐lactalbumin with oleic acid (OA) have been reported to display selective apoptotic activity against tumor cells. These were named (HAMLET) or (BAMLET) alpha‐lactalbumin made lethal Here, we analyzed the OA fragments of obtained limited proteolysis protein. Specifically, investigated 53–103 two‐chain fragment species 1–40/53–123 1–40/104–123, these last being N‐terminal 1–40 covalently linked via disulfide bridges C‐terminal 53–123...
Our objective was to address the balance of inducible nitric oxide (NO) synthase (iNOS) and arginase their contribution contractile dysfunction in heart failure (HF). Excessive NO formation is thought contribute dysfunction; macrophages, increased iNOS expression associated with expression, which competes for arginine. With substrate limitation, may become uncoupled produce reactive oxygen species (ROS). In rabbits, HF induced by left ventricular (LV) pacing (400 beats/min) 3 wk. mRNA...
α-Lactalbumin (LA) forms with oleic acid (OA) a complex which has been reported to induce the selective death of tumor cells. However, mechanism by this kills wide range cell lines is as yet largely unknown. The difficulty in rationalizing cytotoxic effects LA/OA can be due fact that molecular aspects interaction between protein and fatty are still poorly understood, particular regarding oligomeric state actual molar ratio OA over complex. Here, effect LA addition an aqueous solution...
Although mitochondrial dysfunction and oxidative stress have been proposed to play a crucial role in several types of muscular dystrophy (MD), whether causal link between these two alterations exists remains an open question. We documented that through opening the permeability transition pore plays key myoblasts from patients as well mouse models MD, caused by monoamine oxidases (MAO) is involved myofiber damage. In present study we tested MAO-dependent determinant apoptosis affected...
Coenzyme Q (CoQ), a redox-active lipid, is comprised of quinone group and polyisoprenoid tail. It an electron carrier in the mitochondrial respiratory chain, cofactor other dehydrogenases, essential antioxidant. CoQ requires large set enzymes for its biosynthesis; mutations genes encoding these proteins cause primary deficiency, clinically genetically heterogeneous diseases. Patients with deficiency often respond to oral CoQ10 supplementation. Treatment however problematic because low...
Significance We have developed a method for finding pharmaceuticals that would treat obesity and type 2 diabetes by increasing the metabolic rate of resting skeletal muscle. The is increased shifting motor protein myosin from low activity state to higher state. devised an assay, screened compounds, found one molecule, piperine. Piperine muscle fibers. does not properties required be pharmaceutical in humans, but it make good lead compound compounds do. Our results provide proof concept these...
Glutaminolysis is known to correlate with ovarian cancer aggressiveness and invasion. However, how this affects the tumor microenvironment elusive. Here, we show that cells become addicted extracellular glutamine when silenced for synthetase (GS), similar naturally occurring GS-low, glutaminolysis-high cells. Glutamine addiction elicits a crosstalk mechanism whereby release N-acetylaspartate (NAA) which, through inhibition of NMDA receptor, synergistically IL-10, enforces GS expression in...
The mechanism of cell death was investigated in Jurkat cells exposed to the combination psoralen and UVA irradiation (PUVA). Apoptosis by far prevailing over necrosis involved mitochondrial dysfunction. collapse membrane potential, appears be caused opening permeability transition pore since its inhibitor, cyclosporin A, prevented dysfunction largely attenuated apoptosis. also occurred treated with photoproducts generated irradiating vitro an oxygen‐dependent process. Thus, involvement...