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001-es BibID:BIBFORM014050
Első szerző:Kruzel, Marian L.
Cím:Lactoferrin decreases LPS-induced mitochondrial dysfunction in cultured cells and in animal endotoxemia model / Marian L. Kruzel, Jeffrey K. Actor, Zsolt Radak, Attila Bacsi, Alfredo Saavedra-Molina, Istvan Boldogh
Dátum:2010
ISSN:1753-4259
Megjegyzések:Lactoferrin is a non-heme iron-binding glycoprotein, produced by mucosal epithelial cells and granulocytes in most mammalian species. It is involved in regulation of immune responses, possesses anti-oxidant, anti-carcinogenic, anti-inflammatory properties, and provides protection against various microbial infections. In addition, lactoferrin has been implicated in protection against the development of insult-induced systemic inflammatory response syndrome (SIRS) and its progression into septic conditions in vivo. Here we show a potential mechanism by which lactoferrin lessens oxidative insult at the cellular and tissue levels after lipopolysaccharide (LPS) exposure. Lactoferrin pretreatment of cells decreased LPS-mediated oxidative insults in a dose-dependent manner. Lipopolysaccharide-induced oxidative burst was found to be of mitochondrial origin, and release of reactive oxygen species (ROS) was localized to the respiratory complex III. Importantly, lactoferrin nearly abolished LPS-induced increases in mitochondrial ROS generation and the accumulation of oxidative damage in the DNA. In vivo, pretreatment of experimental animals with lactoferrin significantly (P50.05) lowered LPS-induced mitochondrial dysfunction as shown by both decreased release of H2O2 and DNA damage in the mitochondria. In contrast, deferoxamine, an iron chelating compound, provided only partial protection in LPS-treated animals. Together, these data suggest that lactoferrin protects against oxidative insult at the mitochondrial level, and indicate a potential utility of lactoferrin in prevention and treatment of SIRS.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
DNA-DAMAGE
HYDROGEN-PEROXIDE
OXIDATIVE DAMAGE
ROS GENERATION
REPAIR
MECHANISMS
OXIDASES
SEPSIS
DEATH
MTDNA
Megjelenés:Innate Immunity 16 : 2 (2010), p. 67-79. -
További szerzők:Actor, Jeffrey K. Radák Zsolt Bácsi Attila (1967-) (immunológus) Saavedra-Molina, Alfredo Boldogh István
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001-es BibID:BIBFORM076593
Első szerző:Sipka Sándor (laboratóriumi szakorvos)
Cím:Comparison of endotoxin levels in cow's milk samples derived from farms and shops / Sipka Sándor, Béres Andrea, Bertók Lóránd, Varga Tamara, Bruckner Geza
Dátum:2015
ISSN:1753-4259 1753-4267
Megjegyzések:The observations on the protective effect of bacterial endotoxin in farm-derived cow's milk on childhood asthma and allergy are contradictory. The aim of this study was to determine the endotoxin levels in ♭farm-derived whole raw' and ♭processed shop' sources of cow's milk, and to test how the temperature and storing conditions might alter their endotoxin concentrations. Milk was collected from farms and shops. The level of endotoxin was measured by micro (gel-clot) Limulus amebocyte lysate test expressed as EU/ml. The concentration ranges of endotoxin were much higher and more widely scattered in the samples of whole raw farm milk than in the processed shop milk. Cold storage or heating increased the endotoxin concentrations in all samples of farm milk, but not in the processed shop milk. These results show that elevated levels of endotoxin in raw farm milk samples can occur from the cowshed or be formed during storage. In processed shop milk, storage does not cause any changes in the amount of endotoxin. Therefore, it is consistent that the handling and storage of raw milk alters the endotoxin concentrations, which may explain previous contradictory findings regarding the beneficial modulating effects on innate immunity toward allergy prevention in early childhood.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Allergy prevention
cow's milk
endotoxin
temperature dependence
Megjelenés:Innate Immunity. - 21 : 5 (2015), p. 531-536. -
További szerzők:Béres Andrea Bertók Lóránd (1934-) (sugárbiológus, immunológus) Varga Tamara Bruckner Géza
Pályázati támogatás:71883
OTKA
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