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001-es BibID:	BIBFORM002003
Első szerző:	Bácsi Attila (immunológus)
Cím:	Increased ROS generation in subsets of OGG1 knockout fibroblast cells / Attila Bacsi, Grzegorz Chodaczek, Tapas K. Hazra, David Konkel, Istvan Boldogh
Dátum:	2007
Megjegyzések:	Oxoguanine DNA glycosylase (OGG1) is a major base excision repair protein responsible for excision of the mutagenic 8-oxoguanosine (8-oxoG) lesions from the genome. Despite OGG1's importance, the moderate phenotype of Ogg1-null (Ogg1_/_) mice is not well understood. This study addresses a mechanism by which Ogg1_/_ cells limit accumulation of 8-oxoG in their genome. Our data reveal that a subset of Ogg1_/_ cells shows higher ROS levels (HROS cells), while _85% of Ogg1_/_ cells exhibit physiological levels of ROS (LROS cells). Ogg1_/_ cells were sorted based on their DCF fluorescence intensity to obtain LROS and HROS cell cultures. LROS cultures proliferated at a rate comparable to Ogg1+/+ and gradually accumulated cells exhibiting increased ROS and 8-oxoG levels. LROS cells show a 2.8-fold increase in 8-oxoG level vs. HROS cells (7? 27-fold). Mitochondria of HROS cells released more H2O2 than LROS and Ogg1+/+ cells and were eliminated by apoptotic-like processes. These findings suggest that in the absence of OGG1, a surveillance system is activated that removes cells with extreme 8-oxoG levels from Ogg1_/_ cultures. Whether similar mechanisms exists in tissues of Ogg1_/_ mice is the focus of future investigations.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Ogg1 null fibroblast ROS 8-oxoguanine Mitochondria
Megjelenés:	Mechanisms of ageing and development. - 128 : 11-12 (2007), p. 637-649. -
További szerzők:	Chodaczek, Grzegorz Hazra, Tapas K. Konkel, David Boldogh István
Internet cím:	elektronikus változat DOI elektronikus változat
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001-es BibID:	BIBFORM033270
035-os BibID:	WOS:000166627300004 PMID:11163624
Első szerző:	Imre Sándor (pathofiziológus)
Cím:	High sensitivity to autoxidation in neonatal calf erythrocytes : possible mechanism of accelerated cell aging / S. Imre, M. Csornai, M. Balazs
Dátum:	2001
Megjegyzések:	The suspension viscosity, formation of methaemoglobin and production of malondialdehyde (MDA) associated with the non-enzymatic oxidation of polyunsaturated fatty acids during auto-oxidation conditions in vitro have been compared in erythrocytes From young calves (2, 4 and 6 weeks of age) and mature cattle. The autoxidation conditions were designed to simulate the oxidative stress to which neonatal erythrocytes are exposed in vivo. Characterisation of lipid peroxidation was also undertaken by a combination of lipid fluorescent measurements and quantification of the superoxide: dismutase (SOD) activities of the erythrocytes, The results demonstrated that high SOD activities in the erythrocytes of the neonatal calf was insufficient to afford protection against the increased autoxidation of haemoglobin and subsequent accumulation of lipid peroxidation products, High levels of methaemoglobin formation and lipid peroxidation were able to provide an explanation for an observed reduction in rheological adaptability (increased suspension viscosity) and an accelerated aging of the neonatal cells under in vivo conditions.
Tárgyszavak:	Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban Superoxide dismutase Lipid peroxidation Autoxidation Rheology Calf erythrocytes egyetemen (Magyarországon) készült közlemény
Megjelenés:	Mechanisms of ageing and development. - 122 : 1 (2001), p. 69-76. -
További szerzők:	Csornai Márta Balázs Margit (1952-) (sejtbiológus, molekuláris genetikus)
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM053869
Első szerző:	Semsei Imre (vegyész, gerontológus)
Cím:	On the nature of aging / Imre Semsei
Dátum:	2000
ISSN:	0047-6374
Megjegyzések:	Most of the aging theories are monistic in nature, they omit numerous key factors of senescence during the process of model creation. There are two main categories of these theories: program theories and error (mutation) ones. Program theories imply the existence of internal or external programs that determine the aging process ab ovo. The error theories involve explicit or implicit the idea that aging would not happen without the destructive factors that cause errors, mutations, regulation disorders, and in turn these processes finally lead to disfunctions and senescence. The aim of this paper is to indicate that aging may be multifactorial and the process of senescence may be determined by the information level of the organization. This level itself changes during senescence (including the information level of the genom that also alters by time because of, e.g. its 'fluid' character). According to this approach the aging process is determined by the sum effects of internal (e.g. genom) and external (material, energy, information) factors, although there are some elements that bear more importance than others. Subsequently, the maximal life-span is probably determined by the principle of the weakest element of the chain. Because of the high complexity of the human body where different information systems superpose each other, the cooperation of the elements (counter-effects, regulation) have the same determining importance as the information level of the unit parts (cells) have. The further aim of this paper is to show that the roots of certain diseases (e.g. cancer) could firmly be linked to the aging process itself. This interpretation offers two ways of influencing the process of senescence. It could be influenced by maintaining the information level of the organism via optimization or by changing (elevating) this level. All the factors that help to prevent the decrease of the information level of the organism could act against aging and certain diseases, and vice versa: the factors which deteriorate the state of the information system could contribute to the acceleration of the aging process.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Mechanisms of Ageing and Development. - 117 : 1-3 (2000), p. 93-108. -
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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