Putzki H, Reichert B
Klinik und Poliklinik für Allgemeinchirurgie, Medizinischen Hochschule in Hannover.
Gastroenterol J. 1990;50(1):50-2.
The increase of activity of the enzymes AP, Gamma-GT, GlDH and GPT was investigated in this study with regard to its pathomechanism. The increase of AP is known to be caused by a de novo-protein synthesis in the liver, as several investigators have demonstrated using protein synthesis inhibitors. In this study female Wistar rats were partly sham-operated, partly bile duct-obstructed. One half of each group received the protein synthesis inhibitor ethionine, 24 h after bile duct obstruction in the group with ethionine the following enzyme activities were measured in the serum: AP 216 +/- 80 U/l; gamma-GT 4.5 +/- 1.9 U/l; GlDH 85 +/- 26 U/l; GPT 375 +/- 163 U/l. In the group without ethionine the activities were: AP 459 +/- 69 U/l; gamma-GT 4 +/- 0.9 U/l; GlDH 120 +/- 81 U/l; GPT 417 +/- 191 U/l. Because the differences between the groups with and without ethionine were not significant with the exception of AP, it is concluded that in the early phase of bile duct obstruction up to 24 h no influence of de novo-protein synthesis can be demonstrated in the elevation of the activities of gamma-GT, GlDH and GPT.
本研究针对碱性磷酸酶（AP）、γ-谷氨酰转肽酶（Gamma-GT）、谷氨酸脱氢酶（GlDH）和谷丙转氨酶（GPT）活性增加的病理机制展开了研究。正如几位研究者使用蛋白质合成抑制剂所证明的那样，已知AP活性的增加是由肝脏中从头合成蛋白质所致。在本研究中，对雌性Wistar大鼠进行了部分假手术和部分胆管阻塞手术。每组的一半大鼠在胆管阻塞24小时后接受蛋白质合成抑制剂乙硫氨酸处理，在乙硫氨酸组中，于胆管阻塞后测定血清中的下列酶活性：AP为216±80 U/l；γ-GT为4.5±1.9 U/l；GlDH为85±26 U/l；GPT为375±163 U/l。在未使用乙硫氨酸的组中，酶活性分别为：AP为459±69 U/l；γ-GT为4±0.9 U/l；GlDH为120±81 U/l；GPT为417±191 U/l。由于除AP外，使用和未使用乙硫氨酸的组之间差异不显著，因此得出结论，在胆管阻塞至24小时的早期阶段，γ-GT、GlDH和GPT活性升高过程中未显示出从头合成蛋白质的影响。
