Hale W B, Turner B, LaMont J T
Evans Memorial Department of Clinical Research, University Hospital, Boston University School of Medicine, Massachusetts 02118.
Am J Physiol. 1987 Nov;253(5 Pt 1):G627-30. doi: 10.1152/ajpgi.1987.253.5.G627.
In several animal models of cholelithiasis, and in humans with gallstones, hypersecretion of gallbladder mucin is observed. This study was undertaken to determine the effect of oxygen radicals on guinea pig gallbladder glycoprotein secretion in organ culture. Mucosal explants were incubated with [3H]glucosamine hydrochloride to label glycoproteins, then exposed to oxygen radicals generated by chelated ferric iron and ascorbic acid. Marked stimulation of glycoprotein release was observed after a 30-min exposure to the oxygen radical-generating system, and the effect was inhibited by mannitol. The stimulatory effect of hydroxyl radical was not accompanied by leakage of intracellular lactate dehydrogenase. Parallel experiments with human granulocytes activated with f-Met-Leu-Phe and coincubated with gallbladder explants revealed similar results. These results indicate that oxygen radicals, especially the hydroxyl radical (OH.), are capable of stimulating rapid release of mucous-type glycoproteins from gallbladder epithelium.
在几种胆结石动物模型以及患有胆结石的人类中，均观察到胆囊粘蛋白分泌过多。本研究旨在确定氧自由基对器官培养中豚鼠胆囊糖蛋白分泌的影响。将黏膜外植体与盐酸[³H]葡萄糖胺一起孵育以标记糖蛋白，然后暴露于由螯合铁和抗坏血酸产生的氧自由基中。在暴露于产氧自由基系统30分钟后，观察到糖蛋白释放受到显著刺激，且该作用可被甘露醇抑制。羟自由基的刺激作用并未伴随细胞内乳酸脱氢酶的泄漏。用f-Met-Leu-Phe激活并与胆囊外植体共孵育的人粒细胞进行的平行实验也得出了类似结果。这些结果表明，氧自由基，尤其是羟自由基（OH·），能够刺激胆囊上皮细胞快速释放粘液型糖蛋白。
