Lin S R, Chang C C
Department of Chemistry, Kaohsiung Medical College, Taiwan, ROC.
Biochim Biophys Acta. 1992 Oct 20;1159(3):255-61. doi: 10.1016/0167-4838(92)90053-g.
The reaction of alpha-bungarotoxin (alpha-BuTX) with 1,2-cyclohexanedione resulted in the modification of only Arg-72 but arginine at position 36 or 72, as well as both were modified by reaction of the toxin with p-hydroxyphenylglyoxal. No derivative modified at Arg-25 was obtained, indicating that this residue may be located in the interior region of alpha-BuTX molecule. Monoderivative at Arg-72 showed about 50% of the lethal toxicity and binding activity of alpha-BuTX to nicotinic acetylcholine receptor (AChR), while the activity was decreased to one-third when the invariant Arg-36 was modified, indicating that the latter residue is more closely related to the interaction of the toxin with AChR. Approx. 13% of the residual activity was observed when both arginine residues at 36 and 72 were modified. The antigenicity of alpha-BuTX was still retained essentially intact after Arg-36 or -72 was modified, whereas it decreased to 50% when both these arginine residues were modified. The present study indicates that Arg-36 and -72 in alpha-BuTX may be involved in the multipoint contact between the toxin and AChR, but neither is absolutely essential for the binding.
α-银环蛇毒素（α-BuTX）与1,2-环己二酮反应仅导致精氨酸-72发生修饰，但36位或72位的精氨酸，以及毒素与对羟基苯乙二醛反应时两者都会被修饰。未获得在精氨酸-25处修饰的衍生物，这表明该残基可能位于α-BuTX分子的内部区域。精氨酸-72处的单衍生物显示出α-BuTX对烟碱型乙酰胆碱受体（AChR）的致死毒性和结合活性的约50%，而当不变的精氨酸-36被修饰时，活性降至三分之一，这表明后一个残基与毒素与AChR的相互作用关系更密切。当36位和72位的精氨酸残基都被修饰时，观察到约13%的残余活性。在精氨酸-36或-72被修饰后，α-BuTX的抗原性基本仍保持完整，而当这两个精氨酸残基都被修饰时，其抗原性降至50%。本研究表明，α-BuTX中的精氨酸-36和-72可能参与毒素与AChR之间的多点接触，但两者对于结合都不是绝对必需的。
