Di Giacomo C, Sorrenti V, Acquaviva R, Campisi A, Vanella G, Perez-Polo J R, Vanella A
Institute of Biochemistry, University of Catania, Italy.
Neurochem Res. 1997 Sep;22(9):1145-50. doi: 10.1023/a:1027321420075.
Excessive activation of glutamate receptors via the N-methyl-D-aspartate (NMDA) subtype appears to play a role in the sequence of cellular events which lead to irreversible ischemic damage to neurons. Furthermore, NMDA receptor activation induces a stimulation of ornithine decarboxylase (ODC), the rate-limiting enzyme for polyamine (PA) biosynthesis. In order to better understand the role of PA we have measured ODC activity and the effect of methionine sulfoximine (MSO), a molecule able to stimulate ODC, on a model of transient cerebral ischemia. There was a significant increase in ODC activity in the rat cerebral cortex during post-ischemic reperfusion. The treatment with MSO induced a significant decrease in cerebral glutamine synthetase activity accompanied by a marked increase in ODC activity. In MSO-pretreated rats there was a significant decrease in the survival rate when compared to untreated ischemic rats.
通过N-甲基-D-天冬氨酸（NMDA）亚型过度激活谷氨酸受体似乎在导致神经元不可逆性缺血损伤的细胞事件序列中起作用。此外，NMDA受体激活会诱导鸟氨酸脱羧酶（ODC）的刺激，鸟氨酸脱羧酶是多胺（PA）生物合成的限速酶。为了更好地理解PA的作用，我们在短暂性脑缺血模型中测量了ODC活性以及蛋氨酸亚砜亚胺（MSO，一种能够刺激ODC的分子）的作用。缺血后再灌注期间，大鼠大脑皮层的ODC活性显著增加。MSO处理导致脑谷氨酰胺合成酶活性显著降低，同时ODC活性显著增加。与未处理的缺血大鼠相比，MSO预处理的大鼠存活率显著降低。
