海蛇（蓝灰扁尾海蛇）毒液中一种有毒磷脂酶A2及其无毒同源物的神经肌肉效应

Neuromuscular effects of a toxic phospholipase A2 and its nontoxic homologue from the venom of the sea snake, Laticauda colubrina.

作者信息

Rowan E G, Harvey A L, Takasaki C, Tamiya N

机构信息

Department of Physiology and Pharmacology, University of Strathclyde, Glasgow, U.K.

出版信息

Toxicon. 1989;27(5):587-91. doi: 10.1016/0041-0101(89)90120-7.

DOI:10.1016/0041-0101(89)90120-7

PMID:2749757

Abstract

A single chain phospholipase A2 (LcPLA-II) and a homologous protein lacking enzymatic activity (LcPLH-I) isolated from the venom of the Solomon Island sea snake (Laticauda colubrina) were tested for effects on neuromuscular transmission and muscle contractility on chick biventer cervicis and mouse hemidiaphragm preparations. LcPLA-II (7.5 nM-1.5 microM) blocked indirectly elicited muscle contractions of both preparations. Low concentrations of LcPLA-II caused little change in sensitivity to acetylcholine, carbachol and KCl. The homologue LcPLH-I (375 nM-1.5 microM) reduced the responses of the biventer cervicis preparation to indirect stimulation and abolished responses to acetylcholine and carbachol, but it did not block KCl responses. These effects were due to minor contamination by a post-junctional neurotoxin. LcPLH-I (375 nM-750 nM) had no effect on indirectly stimulated hemidiaphragm preparations. It is concluded that LcPLA-II blocks neuromuscular transmission by a prejunctional action, and that the homologue lacking phospholipase A2 activity also lacks neuromuscular activity.

摘要

从所罗门岛海蛇（Laticauda colubrina）毒液中分离出的单链磷脂酶A2（LcPLA-II）和一种缺乏酶活性的同源蛋白（LcPLH-I），在鸡双颈肌和小鼠半膈肌标本上测试了它们对神经肌肉传递和肌肉收缩性的影响。LcPLA-II（7.5 nM - 1.5 microM）阻断了两种标本间接引发的肌肉收缩。低浓度的LcPLA-II对乙酰胆碱、卡巴胆碱和氯化钾的敏感性几乎没有影响。同源蛋白LcPLH-I（375 nM - 1.5 microM）降低了双颈肌标本对间接刺激的反应，并消除了对乙酰胆碱和卡巴胆碱的反应，但它并未阻断对氯化钾的反应。这些影响是由于受到一种接头后神经毒素的轻微污染所致。LcPLH-I（375 nM - 750 nM）对间接刺激的半膈肌标本没有影响。得出的结论是，LcPLA-II通过接头前作用阻断神经肌肉传递，并且缺乏磷脂酶A2活性的同源蛋白也缺乏神经肌肉活性。