Baniukiewicz A A, Dlugosz J W, Gabryelewicz A
Gastroenterology Department, Medical Academy, Bialystok, Poland.
Int J Pancreatol. 1994 Aug;16(1):71-9. doi: 10.1007/BF02925612.
The decompartmentation of lysosomal compartment in pancreatic acinar cells with consecutive activation of zymogens might play an important role as a "trigger mechanism" in acute pancreatitis. The admixture of lysosomal hydrolases to secretory enzymes in pancreatic juice was found, but their role in pancreatic secretion remains obscure. The aim of the present study was to assess the fragility of pancreatic lysosomal structure after maximal (optimal) or supramaximal stimulation of rats with cerulein during 3, 6, 12 h, and after recovery. In the mitochondrial-lysosomal (M-L) and in the supernatant (S) of pancreases free (F) total (T), and fractional free (%F/T) activities of beta-glucuronidase (beta G), acid phosphatase (AcP), cathepsins (Cs), and beta-N-acetyl-hexosaminidase (NAH) were estimated. In edematous pancreatitis following supramaximal stimulation with cerulein, a significant increase of %F/T of beta G in whole homogenate began at 6 h of hyperstimulation in comparison to the control (93 vs 42% p < 0.01). This increment persisted until 12 h of hyperstimulation and declined after 24 and 48 h of recovery to 67-69%. The changes of %F/T of beta G in M-L followed those in whole homogenate, and additionally the increase free activity in S after 6 h of hyperstimulation and after 24 h recovery occurred. The respective activities of other hydrolases showed a similar pattern of changes. It is of interest that fragility of lysosomal membranes increases significantly also after maximal stimulation when inflammatory changes were absent. Our results suggest that the increase of lysosomal fragility of the pancreas is most unlikely pathological in itself, but also occurs during stimulated pancreatic secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
随着酶原的连续激活,胰腺腺泡细胞溶酶体区室的去分隔化可能作为急性胰腺炎的“触发机制”发挥重要作用。研究发现胰液中溶酶体水解酶与分泌酶混合存在,但其在胰腺分泌中的作用仍不清楚。本研究旨在评估用雨蛙肽对大鼠进行最大(最佳)或超最大刺激3、6、12小时及恢复后胰腺溶酶体结构的脆弱性。测定胰腺线粒体 - 溶酶体(M - L)和上清液(S)中游离(F)、总(T)β - 葡萄糖醛酸酶(βG)、酸性磷酸酶(AcP)、组织蛋白酶(Cs)和β - N - 乙酰己糖胺酶(NAH)的活性及游离部分占总活性的百分比(%F/T)。在用雨蛙肽进行超最大刺激后的水肿性胰腺炎中,与对照组相比,超刺激6小时时全匀浆中βG的%F/T显著增加(93%对42%,p < 0.01)。这种增加持续到超刺激12小时,在恢复24和48小时后降至67 - 69%。M - L中βG的%F/T变化与全匀浆一致,此外,超刺激6小时后及恢复24小时后S中游离活性增加。其他水解酶的各自活性也呈现类似的变化模式。有趣(的是),在无炎症变化的最大刺激后,溶酶体膜的脆弱性也显著增加。我们的结果表明,胰腺溶酶体脆弱性的增加本身极不可能是病理性的,而是在刺激的胰腺分泌过程中也会发生。(摘要截短至250字)