Palenker J, Lentzen H, Brandt U
Naunyn Schmiedebergs Arch Pharmacol. 1984 Mar;325(3):214-7. doi: 10.1007/BF00495946.
Degradation of tritiated [Leu5]enkephalin was studied in cultures of neuroblastoma cells (clone N1E-115). Incubation of cells in suspension revealed Tyr as the main tritiated metabolite; however, Tyr-Gly-Gly and Tyr-Gly were detectable as well. In a crude membrane preparation of the neuroblastoma cells the level of Tyr is reduced to 13% and that of Tyr-Gly to 10% of the initial value, whereas Tyr-Gly-Gly is increased to about 5 times the initial value. Of the degraded enkephalin, 66% was accounted for by the formation of Tyr, 30% by the formation of Tyr-Gly-Gly and 4% by the formation of Tyr-Gly. The production of Tyr was inhibited by bestatin, an inhibitor of aminopeptidases, and that of Tyr-Gly-Gly by captopril, an inhibitor of angiotensin-converting-enzyme. The results prove the ability of neuroblastoma cells (N1E-115) to degrade enkephalin by aminopeptidase and the membrane-bound angiotensin-converting-enzyme.
在神经母细胞瘤细胞（克隆N1E - 115）培养物中研究了氚标记的[亮氨酸5]脑啡肽的降解。悬浮培养细胞时，发现酪氨酸是主要的氚标记代谢产物；不过，也可检测到酪氨酸 - 甘氨酸 - 甘氨酸和酪氨酸 - 甘氨酸。在神经母细胞瘤细胞的粗制膜制剂中，酪氨酸水平降至初始值的13%，酪氨酸 - 甘氨酸水平降至初始值的10%，而酪氨酸 - 甘氨酸 - 甘氨酸增加至初始值的约5倍。在降解的脑啡肽中，66%是由酪氨酸的形成所致，30%是由酪氨酸 - 甘氨酸 - 甘氨酸的形成所致，4%是由酪氨酸 - 甘氨酸的形成所致。氨肽酶抑制剂贝司他汀抑制酪氨酸的产生，血管紧张素转换酶抑制剂卡托普利抑制酪氨酸 - 甘氨酸 - 甘氨酸的产生。结果证明神经母细胞瘤细胞（N1E - 115）具有通过氨肽酶和膜结合的血管紧张素转换酶降解脑啡肽的能力。
