Base excision repair activities in organotypic hippocampal slice cultures exposed to oxygen and glucose deprivation
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- 作者：Veslemø ; y Rolseth ; Elise Rundé ; n-Pran ; Christine Gran Neurauter ; Arne Yndestad ; Luisa Luna ; På ; l Aukrust ; Ole Petter Ottersen ; Magnar Bjø ; rå ; s
- 关键词：Base excision repair ; Ischemia ; Hippocampus ; DNA glycosylase ; Oxidative base lesions ; CA1
- 刊名：DNA Repair
- 出版年：2008
- 出版时间：1 June 2008
- 年：2008
- 卷：7
- 期：6
- 页码：869-878
- 全文大小：519 K
文摘
The capacity for DNA repair is likely to be one of the factors that determine the vulnerability of neurons to ischemic stress and may influence the pathological outcome of stroke. In this report, initiation of base excision repair (BER) was assessed by analysis of enzyme activity and gene expression level of DNA glycosylases and AP-endonucleases in rat organotypic hippocampal slice cultures exposed to oxygen and glucose deprivation (OGD) – an in vitro model of stroke. Under basal conditions, AP-endonuclease activity and base removal of ethenoadenine and 8-oxoguanine (8-oxoG) were higher (by ![]()
20–35 % ) in CA3/fascia dentata (FD) than in CA1. Base removal of uracil did not differ between the two hippocampal regions, while removal of 5-hydroxyuracil (5-OHU) was slightly less efficient in CA3/FD than in CA1.