首页> 外文期刊>Toxicon: An International Journal Devoted to the Exchange of Knowledge on the Poisons Derived from Animals, Plants and Microorganisms >Myotoxic activity of an acidic phospholipase A(2) isolated from Lachesis muta (Bushmaster) snake venom
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Myotoxic activity of an acidic phospholipase A(2) isolated from Lachesis muta (Bushmaster) snake venom

机译:酸性磷脂酶A(2)分离自Lachesis muta(布什大师)蛇毒的肌毒性活性。

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An acidic phospholipase A(2) isolated from Lachesis muta snake venom denoted LM-PLA(2), showed neither toxic nor anticoagulant activities in contrast to a potent inhibitory effect of collagen-induced platelet aggregation [Fuly, A.L., Machado, O.L.T., Alves, E.W. and Carlini, C.R., 1997, Thromb. Haemost 78, 1372-1380.]. Now, the myotoxicity induced by LM-PLA2 was investigated by using both in vivo and in vitro experiments. LM-PLA(2) induced in vitro a dose- and time-dependent release of creatine-kinase (CK) from mouse Extensor Digitorium Longus (EDL) muscles and also increased the plasma CK activity in treated animals. Histopathological studies confirm myonecrosis of mouse skeletal muscles as a major effect. Edema could also be seen in muscle tissue. The amino-terminal sequence of LM-PLA(2) (previously reported) indicates an aspartic acid residue located at position 49, together with other conserved amino acids present in the Asp-49 phospholipases, such as Tyr-28, Gly-30, Gly-32, His-48. Chemical modification of the protein moiety was also performed. Histidine alkylation with p-bromophenacyl bromide and lysine acetylation with acetic anhydride, abolished both indirect hemolytic and myotoxic activities of LM-PLA(2). On the other hand. contrarily to what has been observed with several basic myotoxic phospholipases, the myotoxic effect induced by LM-PLA(2) was not abolished by heparin. (C) 2000 Elsevier Science. Ltd. All rights reserved. [References: 30]
机译:分离自Lachesis突变蛇毒的酸性磷脂酶A(2)表示为LM-PLA(2),与胶原蛋白诱导的血小板聚集的有效抑制作用相比,既没有毒性也没有抗凝活性[Fuly,AL,Machado,OLT,Alves ,EW和Carlini,CR,1997年,Thromb。 ,《哈默斯特78》,1372-1380。现在,通过体内和体外实验研究了由LM-PLA2诱导的肌毒性。 LM-PLA(2)在体外诱导小鼠伸指长肌(EDL)肌肉中肌酸激酶(CK)的剂量和时间依赖性释放,并且还增加了治疗动物的血浆CK活性。组织病理学研究证实,小鼠骨骼肌的坏死是主要作用。在肌肉组织中也可见水肿。 LM-PLA(2)的氨基末端序列(先前已报道)指示位于49位的天冬氨酸残基,以及Asp-49磷脂酶中存在的其他保守氨基酸,例如Tyr-28,Gly-30, Gly-32,His-48。还对蛋白质部分进行了化学修饰。用对溴苯甲酰溴进行组氨酸烷基化,用乙酸酐进行赖氨酸乙酰化,消除了LM-PLA(2)的间接溶血和肌毒性。另一方面。与几种基本的肌毒性磷脂酶所观察到的相反,肝素并未消除LM-PLA(2)诱导的肌毒性作用。 (C)2000 Elsevier Science。有限公司。保留所有权利。 [参考:30]

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