Marion J, Wolfe L S
Biochim Biophys Acta. 1979 Jul 27;574(1):25-32. doi: 10.1016/0005-2760(79)90080-8.
To determine the origins of the arachidonic acid released post-mortem in brain tissue, [3H]arachidonic acid was injected by the intracerebro-ventricular route and radioactivity monitored in complex lipids and free arachidonic acid at various times after decapitation. The specific activity of the released arachidonic acid was close to that in the total phospholipid fraction and much lower than that of the neutral lipids. The phospholipid with the closest specific activity to the free arachidonic acid recovered at the end of the post-mortem period was phosphatidylinositol. Phosphatidylcholine showed a small but significant decrease in radioactivity post-mortem and could contribute 37% of the arachidonic acid released to the free fatty acid fraction. Arachidonic acid released in rat forebrain after decapitation thus comes from a mixture of phospholipids with phosphatidylinositol and phosphatidylcholine being the major source. Phosphatidylserine and phosphatidic acid did not make important contributions to the free arachidonic acid. In the microsomal fraction, the specific activity of the free arachidonic acid was very close to that in phosphatidylinositol.
为了确定脑组织死后释放的花生四烯酸的来源,通过脑室内途径注射[3H]花生四烯酸,并在断头后的不同时间监测复合脂质和游离花生四烯酸中的放射性。释放的花生四烯酸的比活性接近总磷脂部分中的比活性,远低于中性脂质中的比活性。死后末期回收的与游离花生四烯酸比活性最接近的磷脂是磷脂酰肌醇。磷脂酰胆碱在死后放射性有小幅但显著的下降,并且可以为释放到游离脂肪酸部分的花生四烯酸贡献37%。因此,断头后大鼠前脑释放的花生四烯酸来自磷脂的混合物,其中磷脂酰肌醇和磷脂酰胆碱是主要来源。磷脂丝氨酸和磷脂酸对游离花生四烯酸没有重要贡献。在微粒体部分,游离花生四烯酸的比活性与磷脂酰肌醇中的比活性非常接近。