Kitamura M, Sakaguchi S, Sakaguchi G
J Bacteriol. 1969 Jun;98(3):1173-8. doi: 10.1128/jb.98.3.1173-1178.1969.
The pathogenesis of type E botulism is discussed as an aspect of the physicochemical and biological properties of 12S toxins (prototoxin and trypsin-activated 12S toxin) and the Ealpha and Ebeta components of each 12S toxin. A molecular weight of 350,000 was determined for each 12S toxin and 150,000 for Ealpha and Ebeta. Owing to the structure comprising the subunits Ealpha and Ebeta, 12S toxins are much more stable than Ealpha at low pH values and high temperatures. Such was also the case with type A 19S toxin and its alpha component. The Ealpha component alone accounts for the total toxicity of type E toxin. The toxic substance detected in the blood of the animals administered 12S toxins orally or parenterally was identified as Ealpha from the molecular size and the chromatographic pattern. Prototoxin escaping from detoxification in the stomach owing to the subunit structure may undergo dissociation in the intestine to release the Ealpha component. After absorption, the activated Ealpha appeared in the circulating blood without any further signs of dissociation or enzymatic digestion.
作为12S毒素（原毒素和胰蛋白酶激活的12S毒素）以及每种12S毒素的Eα和Eβ组分的物理化学和生物学特性的一个方面，对E型肉毒中毒的发病机制进行了讨论。测定出每种12S毒素的分子量为350,000，Eα和Eβ的分子量为150,000。由于由Eα和Eβ亚基组成的结构，12S毒素在低pH值和高温下比Eα稳定得多。A型19S毒素及其α组分也是如此。单独的Eα组分构成E型毒素的全部毒性。从经口或经肠外给予12S毒素的动物血液中检测到的有毒物质，从分子大小和色谱图鉴定为Eα。由于亚基结构而在胃中逃避解毒的原毒素可能在肠道中解离以释放Eα组分。吸收后，活化的Eα出现在循环血液中，没有任何进一步解离或酶消化的迹象。
