1,721,204 research outputs found
Redox systems, oxidative stress, and antioxidant defences in health and disease
Reactive oxygen and nitrogen species (RONS) play a key role in the regulation of
cell survival.
While adequate levels of RONS are essential to sustain cell proliferation and survival,
disruption of the endocellular redox state induces cell dysfunction and death. Indeed,
under physiological conditions, a balance between the generation and elimination of RONS
ensures the proper function of redox-sensitive signalling proteins. Conversely, alterations
to the redox homeostasis may disrupt the function of key transcription factors, signaltransduction
pathways and cell-death regulators. Along these lines, understanding the
mechanisms underlying cellular redox homeostasis may help to develop nutraceutical
and/or pharmacological tools to counteract the development of a wide number of redoxdependent
pathologies, including cardiovascular, neurodegenerative, inflammatory-based
diseases and cancer.
The special issue has brought together updated research concerning molecular mechanisms
underlying the control of redox-regulated cell systems in physiological processes
and pathological conditions. In addition, recent evidence on the role of phytochemicals,
nutraceuticals and dietary patterns in the control of redox-dependent pathophysiological
conditions has also been included. New information has been added to this field by means
of 15 articles, with 11 original papers and 4 reviews. [...]
Antioxidant and anti-inflammatory properties of plants extract
Inflammation is an adaptive response triggered by noxious stimuli and conditions such as infection and tissue injury [...]
Topology and energy transport in networks of interacting photosynthetic complexes
We address the role of topology in the energy transport process that occurs in networks of photosynthetic complexes. We take inspiration from light-harvesting networks present in purple bacteria and simulate an incoherent dissipative energy transport process on more general and abstract networks, considering both regular structures (Cayley trees and hyperbranched fractals) and randomly generated ones. We focus on the the two primary light-harvesting complexes of purple bacteria, i.e., the LH1 and LH2, and we use network-theoretical centrality measures in order to select different LH1 arrangements. We show that different choices cause significant differences in the transport efficiencies, and that for regular networks, centrality measures allow us to identify arrangements that ensure transport efficiencies which are better than those obtained with a random disposition of the complexes. The optimal arrangements strongly depend on the dissipative nature of the dynamics and on the topological properties of the networks considered, and depending on the latter, they are achieved by using global versus local centrality measures. For randomly generated networks, a random arrangement of the complexes already provides efficient transport, and this suggests the process is strong with respect to limited amount of control in the structure design and to the disorder inherent in the construction of randomly assembled structures. Finally, we compare the networks considered with the real biological networks and find that the latter have in general better performances, due to their higher connectivity, but the former with optimal arrangements can mimic the real networks' behavior for a specific range of transport parameters. These results show that the use of network-theoretical concepts can be crucial for the characterization and design of efficient artificial energy transport networks. © 2012 American Physical Society
Quantum discord andclassical correlations in the bond-charge Hubbard model: Quantum phasetransitions, off-diagonal long-range order, and violation of themonogamy property for discord
Redox regulation of metabolic syndrome: From biochemical mechanisms to nutritional interventions
According to its "harmonized" definition, metabolic syndrome (MetS) is described as a cluster of metabolic factors that increases the risk of cardiovascular diseases, diabetes (DM) and associated morbidities such as dementia [...]
Betanin inhibits myeloperoxidase/nitrite-mediated peroxidation of low density lipoprotein.
BETANIN INHIBITS MYELOPEROXIDASE/NITRITE-MEDIATED PEROXIDATION OF HUMAN LOW-DENSITY LIPOPROTEIN
M. Allegra, L. Tesoriere, D. Butera, A.M. Pintaudi, M.A. Livrea
Dipartimento Farmacochimico Tossicologico e Biologico - Facoltà di Farmacia - Università di Palermo - Via C. Forlanini 1 - 90134 Palermo
INTRODUCTION: Betanin, the betalain red pigment occurring in the Cariophillalae order plants, including cactus pear, has recently been reported to posses reducing properties and to behave as lipoperoxyl radical-scavenger in vitro (1). In addition, this phytochemical is bioavailable, accumulates in human LDL after ingestion of cactus pear fruits, and is able to protect LDL against copper-induced oxidation in vitro (2,3). Myeloperoxidase (MPO) has been implicated in the in vivo LDL modification and atherogenesis (4). The enzyme, in the presence of nitrite, generates two powerful oxidizing agents, the tyrosyl radical and the nitrosyl one, both of which promote LDL lipid oxidation (4). Taking all this into account we have decided to investigate weather betanin could counteract MPO/nitrite-induced oxidation of LDL.
MATERIALS AND METHODS: Human MPO was purchased from Calbiochem and Glucose oxidase from Sigma. All other chemical and solvents were purchased from Sigma Aldrich or Merck. Preparation of LDL. LDL was prepared from blood serum of healthy volunteers according to Kleinveld et al. (5) with minor modification and stored in the presence of 4mM EDTA at -80°C. Lipid peroxidation of LDL. Reactions were carried out according to Kostyuk et al. (6).
RESULTS: Our results, indicate that betanin is able to inhibit the MPO/nitrite-induced LDL lipid peroxidation, in a dose-dependent manner in the range 1 to 10 μM (Fig.1). We have compared the effectiveness of betanin with that of two well-known physiological antioxidants: α-tocopherol and ascorbic acid. As reported (4), α-tocopherol, the most powerful radical-scavenger, is only able to partially protect LDL lipids from oxidation by the MPO/nitrite system and has scarce or no effect on the powerful hydrophilic oxidants generated by nitrite. On the contrary, vitamin C, which is able to scavenge the peroxidase-generated nitrating species, was very efficient in counteracting the MPO/nitrite-sustained lipid peroxidation. Betanin, was even more effective than vitamin C, at inhibiting the oxidative damage to LDL. The IC50 calculated for betanin (1.4 μM) was more than 10-fold lower than that for ascorbic acid (15.6 μM).
Nitrite, an oxidation product of nitric oxide metabolism, and MPO are considered mediators of the LDL oxidation process in vivo. Our study shows that betanin, a phytochemical occurring in the cactus pear fruit, is able to protect LDL, in an experimental set-up of physiological relevance. In addition, the molecule acts at micromolar concentrations, and appears much more effective than ascorbic acid. Our data collectively indicate a favourable modulation of the oxidation process of LDL and may contribute to the supposed beneficial effect of cactus fruit (2).
1. Lievrea M.A. et al. (2003) in Herbal Medicines, Marcel Dekker, Inc. 537-556.
2. Tesoriere L. et al. The American Journal of Clinical Nutrition (in press).
3. Tesoriere L. et al. (2003). Free Radical Research 37, 689-696.
4. Carr A.C. et al. (2000). Arterioscler Thromb Vasc Biol. 1716-1723.
5. Kleinveld, H.A. et al. (1992). Clin. Chem. 38, 2066-2072.
6. Kostyuk V.A. et al. (2003) FEBS Letters 537:146-50.
7. Kleinveld H.A. et al. (1992). Clinical Chemistry, 38. 2006-2072.
8. Kostyuk V.A. et al. (2003). FEBS Letters, 146-153
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