Herzlich B C, Herbert V
Am J Gastroenterol. 1985 Nov;80(11):841-52.
We found in four of five pernicious anemia gastric juices a partly degraded R binder which was cobalamin specific and has an apparent molecular weight of 60-70,000 daltons. Twenty-nine to 74% (4.8-27.0 ng/ml) of the corrinoid binding capacity could not be blocked by cobinamide (a noncobalamin corrinoid). The fifth pernicious anemia gastric juice and five nonpernicious anemia gastric juices had minimal amounts of this binder (2.5 and 2.2 +/- 1.4 ng/ml). Scatchard analysis revealed that cobalamin-specific R binder has 1000-fold lower affinity for cobinamide than cobalamin. Increasing quantities of trypsin and/or chymotrypsin digested increasing amounts of saliva R binder and an increasing percentage of the remaining digest-resistant R binder acquired cobalamin specificity. Partly degraded R binder in pernicious anemia gastric juice was resistant to further proteolysis. Cobalamin-specific R binder, perhaps produced in vivo by the action of refluxed pancreatic enzymes on swallowed R would preferentially bind ingested and/or biliary cobalamin rather than analogue and thereby could play a role in hastening the development of cobalamin deficiency in pernicious anemia.
我们在五份恶性贫血胃液中的四份里发现了一种部分降解的R结合蛋白，它对钴胺素具有特异性，表观分子量为60 - 70,000道尔顿。29%至74%（4.8 - 27.0纳克/毫升）的类咕啉结合能力不能被钴胺酰胺（一种非钴胺素类咕啉）阻断。第五份恶性贫血胃液和五份非恶性贫血胃液中这种结合蛋白的含量极少（分别为2.5和2.2±1.4纳克/毫升）。斯卡查德分析表明，钴胺素特异性R结合蛋白对钴胺酰胺的亲和力比对钴胺素的亲和力低1000倍。越来越多的胰蛋白酶和/或糜蛋白酶消化了越来越多的唾液R结合蛋白，并且剩余的抗消化R结合蛋白中越来越大比例的部分获得了钴胺素特异性。恶性贫血胃液中部分降解的R结合蛋白对进一步的蛋白水解具有抗性。钴胺素特异性R结合蛋白可能是由反流的胰腺酶作用于吞咽的R结合蛋白在体内产生的，它会优先结合摄入的和/或胆汁中的钴胺素而非类似物，从而可能在加速恶性贫血中钴胺素缺乏的发展方面发挥作用。
