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认识到脲酶的致病性以及持续长期治疗的必要性。

Awakenings to the pathogenicity of urease and the requirement for continuous long term therapy.

作者信息

LeVeen H H, LeVeen E G, LeVeen R F

机构信息

Department of Surgery, Medical University of South Carolina, Charleston.

出版信息

Biomed Pharmacother. 1994;48(3-4):157-66. doi: 10.1016/0753-3322(94)90104-x.

DOI:10.1016/0753-3322(94)90104-x
PMID:7993980
Abstract

Urease is an enzyme found in plants and bacteria, but not mammals. It catalyzes the conversion of urea to carbon dioxide and ammonia. Ammonia shortens the life span of cells; and higher concentrations cause tissue necrosis and cytolysis. Twenty percent of total body urea is converted to ammonia by bacterial urease in the colon. Small injections of urease immunize animals by producing antiurease, a gamma globulin, which inactivates urease. Immunization eliminates the colonic conversion of urea to ammonia. Injection of urease produces ammonia intoxication making immunization hazardous. Although previously impossible, a non enzymatic urease antigen was synthesized by covalently bonding jack bean urease with glutaraldehyde. This antigen stimulated the production of antiurease that inactivates native urease. Helicobacter pylori, a potent urease producer, has been implicated in peptic ulcer, gastritis and other inflammatory bowel lesions. The pathogenicity of H pylori is dependent on its urease production. Immunization to urease can render H pylori non pathogenic. Cirrhotics develop encephalopathy and hyperammonemia because their livers fail to convert all the ammonia in portal venous blood to urea and collaterals develop by passing the liver. Colonic ammonia increases the turnover rate of colonic mucosa. Ammonia absorbed into the portal venous system is transported to the liver where it is reconverted to urea. Absorbed ammonia adversely influences liver function. Infections with urease producing organisms destroy the renal parenchyma and produce struvite stones. Urease immunization aids colonic healing and prevents uremic colitis. Absorbed ammonia is a noxious influence on the liver. Animals immunized to urease regenerate the liver faster and are less susceptible to hepatotoxins. Immunization to urease ameliorates cirrhosis. Proteus and other urease producers become non toxic and do not damage the renal parenchyma. Urease is responsible for the pathogenicity of infections with urease producing organisms. Immunization to urease renders urease producing organisms non pathogenic.

摘要

脲酶是一种存在于植物和细菌中,但不存在于哺乳动物体内的酶。它催化尿素转化为二氧化碳和氨。氨会缩短细胞寿命;较高浓度会导致组织坏死和细胞溶解。结肠中20%的全身尿素会被细菌脲酶转化为氨。小剂量注射脲酶可通过产生抗脲酶(一种γ球蛋白)使动物产生免疫,该抗脲酶会使脲酶失活。免疫可消除结肠中尿素向氨的转化。注射脲酶会导致氨中毒,使得免疫具有危险性。尽管以前无法实现,但通过将刀豆脲酶与戊二醛共价结合,合成了一种非酶脲酶抗原。这种抗原刺激产生抗脲酶,从而使天然脲酶失活。幽门螺杆菌是一种强大的脲酶产生菌,与消化性溃疡、胃炎及其他炎症性肠病病变有关。幽门螺杆菌的致病性取决于其脲酶的产生。对脲酶进行免疫可使幽门螺杆菌失去致病性。肝硬化患者会出现肝性脑病和高氨血症,因为他们的肝脏无法将门静脉血中的所有氨转化为尿素,且侧支循环绕过肝脏形成。结肠氨会增加结肠黏膜的更新率。吸收进入门静脉系统的氨被输送到肝脏,在那里它会重新转化为尿素。吸收的氨会对肝功能产生不利影响。感染产生脲酶的生物体可破坏肾实质并产生鸟粪石结石。脲酶免疫有助于结肠愈合并预防尿毒症性结肠炎。吸收的氨对肝脏有有害影响。对脲酶进行免疫的动物肝脏再生更快,且对肝毒素的敏感性更低。对脲酶进行免疫可改善肝硬化。变形杆菌和其他产生脲酶的生物体变得无毒,不会损害肾实质。脲酶是产生脲酶的生物体感染致病性的原因。对脲酶进行免疫可使产生脲酶的生物体失去致病性。

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