Apurinic and/or apyrimidinic (AP) sites were excised from PM2 phage DNA by two enzymes: an AP endodeoxyribonuclease isolated from rat neocortex chromatin and a rat brain exodeoxyribonuclease, DNase B 111. The resulting gap was filled with DNA polymerase / 3 prepared from rat liver and finally ligated by Escherichiu coli DNA ligase.A repair of DNA damage in nondividing long-lived brain cells appears to be of prime importance for maintaining the functional integrity of a genome. The stability of the DNA repair machinery is expected to provide normal functioning of the mammalian central nervous system. Indeed there is a relationship between the magnitude of the defect in excision DNA repair pathways and neurological abnormalities in patients with genetic diseases [l -31. The most common DNA damage is apurinic and/or apyrimidinic (AP) lesions. The AP lesions in DNA may result from spontaneous depurination [4], from exposure to different chemical and physical agents [5] or from the action of various DNA glycosylase activities, which remove altered bases from DNA [6]. Mammalian enzymes, which can immediately participate in the processes of the excision DNA repair of AP sites, were found in rat liver HeLa cells [12], human placenta [13 -151, human fibroblasts [16] and calf thymus [17], however, a set of analogous enzymes observed in the brain is very deficient [18,19]. Cerebral DNA polymerases and DNA ligases have only been studied sufficiently to shown that they are similar to those from other mammalian tissues [19]. At the same time, data suggest some specificity of DNA repair in cerebral cells [20 -221 which may be due to a short DNA repeat length of chromatin nucleosomal structure in neurons, unique in higher eukaryotic cells [23, 241 and the loss of DNA polymerase a [25] involved in repair pathways of some DNA damage [26]. Tissue specificity of brain DNA repair suggests the presence in the brain of repair enzymes possessing some special properCorrespondence to V. A. Ivanov,
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