Rabin O, Deutsch J, Grange E, Pettigrew K D, Chang M C, Rapoport S I, Purdon A D
Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892-1582, U.S.A.
J Neurochem. 1997 May;68(5):2111-8. doi: 10.1046/j.1471-4159.1997.68052111.x.
Transient global cerebral ischemia affects phospholipid metabolism and features a considerable increase in unesterified fatty acids. Reincorporation of free fatty acids into membrane phospholipids during reperfusion following transient ischemia depends on conversion of fatty acids to acyl-CoAs via acyl-CoA synthetases and incorporation of the acyl group into lysophospholipids. To study the effect of ischemia-reperfusion on brain fatty acid and acyl-CoA pools, the common carotid arteries were tied for 5 min in awake gerbils, after which the ligatures were released for 5 min and the animals were killed by microwave irradiation. Twenty percent of these animals (two of 10) were excluded from the ischemia-reperfusion group when it was demonstrated statistically that brain unesterified arachidonic acid concentration was not elevated beyond the range of the control group. Brain unesterified fatty acid concentration was increased 4.4-fold in the ischemic-reperfused animals, with stearic acid and arachidonic acid increasing the most among the saturated and polyunsaturated fatty acids, respectively. The total acyl-CoA concentration remained unaffected, indicating that reacylation of membrane lysophospholipids is maintained during recovery. However, there was a substantial increase in the stearoyl- and arachidonoyl-CoA and a marked decrease in palmitoyl- and docosahexaenoyl-CoA. These results suggest that unesterified fatty acid reacylation into phospholipids is reprioritized according to the redistribution in concentration of acyl-CoA molecular species, with incorporation of stearic acid and especially arachidonic acid being favored.
短暂性全脑缺血会影响磷脂代谢，其特征是未酯化脂肪酸大量增加。短暂性缺血后再灌注期间，游离脂肪酸重新掺入膜磷脂中，这取决于脂肪酸通过酰基辅酶A合成酶转化为酰基辅酶A，以及酰基掺入溶血磷脂中。为了研究缺血再灌注对脑脂肪酸和酰基辅酶A池的影响，在清醒的沙鼠中结扎双侧颈总动脉5分钟，之后松开结扎线5分钟，然后通过微波辐射处死动物。当统计学证明脑未酯化花生四烯酸浓度未升高至超出对照组范围时，这些动物中有20%（10只中的2只）被排除在缺血再灌注组之外。缺血再灌注动物的脑未酯化脂肪酸浓度增加了4.4倍，其中硬脂酸和花生四烯酸在饱和脂肪酸和多不饱和脂肪酸中增加最多。总酰基辅酶A浓度未受影响，这表明在恢复过程中膜溶血磷脂的再酰化得以维持。然而，硬脂酰辅酶A和花生四烯酰辅酶A大幅增加，而棕榈酰辅酶A和二十二碳六烯酰辅酶A显著减少。这些结果表明，根据酰基辅酶A分子种类浓度的重新分布，未酯化脂肪酸重新酰化进入磷脂的过程被重新排序，硬脂酸尤其是花生四烯酸的掺入受到青睐。
