Eng S P, Lo C S
Department of Physiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799.
Cell Biol Toxicol. 1990 Jan;6(1):95-104. doi: 10.1007/BF00135029.
Mechanisms of cell death induced by toxins probably involve one or more processes such as inhibition of protein synthesis and impairment of plasma membrane integrity leading to an increase in membrane permeability. Since one of the possible actions of mastoparan, a cationic tetradecapeptide from wasp venom, is to perturb membrane phospholipids resulting in an increase in membrane permeability, we studied the effect of chemically synthesized mastoparan on lactate dehydrogenase release (LDH), ethidium bromide and fluorescein accumulation in Madin-Darby Canine Kidney (MDCK) cultured cells. Our results demonstrated that mastoparan induced cytosolic LDH release, ethidium bromide accumulation and intracellular fluorescein depletion in MDCK cells. Neomycin, a polycationic aminoglycoside, interacts with anionic polyphosphoinositides at the plasma membrane. Since both mastoparan and neomycin are cationic peptides and react with the negatively charged membrane phospholipids, we studied the interaction of these two peptides on membrane permeability. Our results demonstrated that neomycin inhibited mastoparan-induced LDH release, ethidium bromide accumulation and intracellular fluorescein depletion.
毒素诱导细胞死亡的机制可能涉及一个或多个过程，如抑制蛋白质合成和损害质膜完整性，导致膜通透性增加。由于来自黄蜂毒液的阳离子十四肽马斯托帕拉（mastoparan）的一种可能作用是扰乱膜磷脂，导致膜通透性增加，我们研究了化学合成的马斯托帕拉对Madin-Darby犬肾（MDCK）培养细胞中乳酸脱氢酶释放（LDH）、溴化乙锭和荧光素积累的影响。我们的结果表明，马斯托帕拉诱导MDCK细胞胞质LDH释放、溴化乙锭积累和细胞内荧光素消耗。新霉素是一种聚阳离子氨基糖苷，在质膜上与阴离子多磷酸肌醇相互作用。由于马斯托帕拉和新霉素都是阳离子肽，且都与带负电荷的膜磷脂反应，我们研究了这两种肽对膜通透性的相互作用。我们的结果表明，新霉素抑制了马斯托帕拉诱导的LDH释放、溴化乙锭积累和细胞内荧光素消耗。
