Tobita M, Nagano I, Nakamura S, Itoyama Y, Kogure K
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Neurosci Lett. 1995 Nov 17;200(2):129-32. doi: 10.1016/0304-3940(95)12097-n.
Using an in situ nick translation procedure, DNA single-strand breaks (SSB) in postischemic gerbil hippocampus were investigated after 15-min forebrain ischemia followed by 0-4h of recirculation. In the control group, increased SSB were noticed in the ependymal cell layer and the dentate gyrus. After 15-min ischemia without recirculation, no remarkable changes in SSB were observed. However, after 1 h of recirculation, a marked increase in SSB was recognized throughout the hippocampus, especially in the cells in CA1 subfield and the dentate gyrus. After 4 h of recirculation, SSB decreased to a level near that of the control group. The results of the present study indicate that ischemic insults may injure intranuclear DNA during postischemic recirculation periods. Although many factors may be involved, activated endonuclease due to an intracellular Ca2+ rise, free radicals, and postischemic hyperthermia appear to be involved in this phenomenon.
采用原位缺口平移法,对前脑缺血15分钟后再灌注0 - 4小时的沙土鼠缺血后海马区DNA单链断裂(SSB)进行了研究。在对照组中,室管膜细胞层和齿状回中SSB增加。缺血15分钟未再灌注时,未观察到SSB有明显变化。然而,再灌注1小时后,整个海马区SSB明显增加,尤其是CA1亚区和齿状回的细胞。再灌注4小时后,SSB降至接近对照组的水平。本研究结果表明,缺血性损伤可能在缺血后再灌注期间损伤核内DNA。尽管可能涉及许多因素,但细胞内Ca2+升高激活的核酸内切酶、自由基和缺血后高热似乎与这一现象有关。