Pediconi M F, Rodriguez de Turco E B, Bazan N G
Neurochem Res. 1983 Jul;8(7):835-45. doi: 10.1007/BF00964544.
The effect of postdecapitation ischemia on the labeling of the free fatty acid pool and their incorporation in lipids was examined during the first 10 min after decapitation in mouse brain that had been injected intracerebrally with either [1-14C]arachidonic acid or [1-14C]palmitic acid. One min after decapitation, animals injected with labeled arachidonic acid exhibited a greatly reduced incorporation of label in brain phospholipids, diglycerides, and triglycerides. When radioactive palmitic acid was used, brain lipids exhibited considerably less inhibition of label. However, a similar degree of inhibition was observed 10 min after decapitation with both fatty acids. At this time, free arachidonic acid had decreased 84% as compared to the 24% decrease observed in the controls, and about 77% of the free palmitic acid remained in the free fatty acid fraction as compared with 30% in the controls. This decreased labeling may reflect ATP shortage that affects the fatty acid activation-reacylation reactions or the enzymes involved. Alternatively, the enhanced endogenous free arachidonic acid may compete with the radiolabeled arachidonic acid resulting in an inhibition of lipid labeling. Inhibition of label may have been greater in radiolabeled arachidonic acid than palmitic because of the larger accumulation of the former endogenous fatty acid during early ischemia.
在向小鼠脑内注射[1-¹⁴C]花生四烯酸或[1-¹⁴C]棕榈酸后，于断头后的最初10分钟内，研究了断头后缺血对游离脂肪酸池标记及其掺入脂质的影响。断头后1分钟，注射标记花生四烯酸的动物脑磷脂、甘油二酯和甘油三酯中标记物的掺入显著减少。当使用放射性棕榈酸时，脑脂质对标记物的抑制作用明显较小。然而，断头后10分钟，两种脂肪酸均观察到相似程度的抑制。此时，游离花生四烯酸减少了84%，而对照组减少了24%；与对照组的30%相比，约77%的游离棕榈酸仍留在游离脂肪酸部分。这种标记减少可能反映了影响脂肪酸活化-再酰化反应或相关酶的ATP短缺。或者，内源性游离花生四烯酸的增加可能与放射性标记的花生四烯酸竞争，导致脂质标记受到抑制。由于前者内源性脂肪酸在早期缺血期间积累更多，放射性标记的花生四烯酸中的标记抑制可能比棕榈酸更大。
