Finkelstein S D, Gilfor D, Farber J L
J Lipid Res. 1985 Jun;26(6):726-34.
The metabolism of lipids in the ischemic liver has been examined in the attempt to define the cause of the previously described loss of phospholipid and to determine whether additional alterations occur that may be related to the disturbances in membrane function. With 3 hr of ischemia, 30% of the cellular phospholipid was lost when measured either as phosphate in a lipid extract of the whole liver or as fatty acyl esters after separation by thin-layer chromatography of the major lipid classes in the same extracts. All phospholipid species were equally affected, and there was no accumulation of lysophospholipids. The loss of phospholipid acyl chains was not accompanied by an increased number of acyl esters as mono-, di-, or triglycerides. There was no increase in the size of the free fatty acid pool, and the content of long chain acyl CoA esters decreased by 50%. The acyl chain composition of the free fatty acid and neutral lipid pools changed, however, to resemble more closely that of the phospholipids. There was no change in the fatty acid composition of the phospholipids. The incorporation of intraportally injected [3H]arachidonic acid into total phospholipids was decreased upon reperfusion of liver that had been ischemic for only 20 min. These data are consistent with a loss of fatty acyl chains from the phospholipids into the free fatty acid pool. A few of these chains are incorporated into neutral lipids, but most are lost from the liver.(ABSTRACT TRUNCATED AT 250 WORDS)
为了确定先前所述磷脂丢失的原因,并确定是否发生了可能与膜功能紊乱相关的其他改变,研究人员对缺血肝脏中的脂质代谢进行了检测。缺血3小时后,以全肝脂质提取物中的磷酸盐来衡量,或者以同一提取物中主要脂质类经薄层色谱分离后的脂肪酰酯来衡量,细胞磷脂损失了30%。所有磷脂种类均受到同等影响,且溶血磷脂没有积累。磷脂酰链的丢失并未伴随着单酰甘油、二酰甘油或三酰甘油等酰酯数量的增加。游离脂肪酸池的大小没有增加,长链酰基辅酶A酯的含量下降了50%。然而,游离脂肪酸和中性脂质池的酰链组成发生了变化,更类似于磷脂的组成。磷脂的脂肪酸组成没有变化。在仅缺血20分钟的肝脏再灌注时,经门静脉注射的[3H]花生四烯酸掺入总磷脂的量减少。这些数据与磷脂中的脂肪酰链向游离脂肪酸池的丢失一致。其中一些链被掺入中性脂质中,但大多数从肝脏中丢失。(摘要截选至250词)