Chitolina Schetinger M R, Bonan C D, Schierholt R C, Webber A, Arteni N, Emanuelli T, Dias R D, Freitas Sarkis J J, Netto C A
Departamento de Química, Universidade Federal de Santa Maria, Santa Maria, Brasil.
J Stroke Cerebrovasc Dis. 1998 Sep-Oct;7(5):281-6. doi: 10.1016/s1052-3057(98)80044-x.
Adenosine, an endogenous neuroprotective agent, can be produced in the synaptic cleft from adenosine triphosphate (ATP) hydrolysis via the concerted action of two enzymes: ATP diphosphohydrolase and 5'-nucleotidase. The aim of the present study was to investigate such enzymatic activities in the hippocampus of rats subjected to single (2- or 10-minute) or double (2+10 minute, with a 24-hour interval in between, named preconditioned group) ischemic episodes. Ischemia was produced by four-vessel occlusion method. Histological analysis showed no cell death in 2-minute ischemia, and up to 90% of pyramidal CA(1) cell loss in the 10-minute ischemic group. As predicted, double ischemic rats displayed a significant cytoprotective effect (around 60%). Preconditioned rats presented a delayed enhancement in ATP diphosphohydrolase activity (for ATP and adenosine diphosphate hydrolysis) after 48 hours of reperfusion. 5'-nucleotidase activity was increased immediately after ischemic insult (for all groups) and after a late reperfusion period (48 hours). We suggest that preconditioning causes delayed changes in enzymatic activities that would conceivably lead to increased adenosine production. This effect could be related to cytoprotection seen in preconditioned rats.
腺苷是一种内源性神经保护剂，可在突触间隙由三磷酸腺苷（ATP）通过两种酶的协同作用水解产生：ATP二磷酸水解酶和5'-核苷酸酶。本研究的目的是调查单次（2分钟或10分钟）或两次（2 + 10分钟，中间间隔24小时，称为预处理组）缺血发作的大鼠海马中的这种酶活性。缺血通过四血管闭塞法产生。组织学分析显示，2分钟缺血组无细胞死亡，10分钟缺血组高达90%的锥体CA(1)细胞丢失。正如预期的那样，两次缺血的大鼠表现出显著的细胞保护作用（约60%）。预处理的大鼠在再灌注48小时后，ATP二磷酸水解酶活性（用于ATP和二磷酸腺苷水解）出现延迟增强。5'-核苷酸酶活性在缺血损伤后立即（所有组）以及再灌注后期（48小时）增加。我们认为预处理会导致酶活性的延迟变化，这可能会导致腺苷生成增加。这种效应可能与预处理大鼠中观察到的细胞保护作用有关。
