Találati lista | Tudóstér

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
Borító:
Saját polcon: