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感染兔痘病毒的HeLa细胞中血浆膜和溶酶体膜的通透性变化

Permeability changes of plasma and lysosomal membranes in HeLa cells infected with rabbit poxvirus.

作者信息

Schümperli D, Peterhans E, Wyler R

出版信息

Arch Virol. 1978;58(3):203-12. doi: 10.1007/BF01317602.

Abstract

Infection of HeLa-cell monolayer cultures with rabbit poxvirus induces a marked decrease in cell-associated protein and in the activities of lactate dehydrogenase, acid phosphatase, and beta-glucuronidase. This effect begins to occur around 10 hours post-infection (p.i.) and is accompanied by a concomitant rise of these enzyme activities in the culture medium. Only few cells detach from infected monolayers and these cannot account for protein release. Virion release can be inhibited at 4 degrees C, whereas protein release cannot and it seems therefore that these events do not happen by a common mechanism. Moreover, penetration studies with [14C]-sucrose indicate that protein release reflects a true increase in plasma membrane permeability. Using the Gomori stain for acid phosphatase, a release of the enzyme into the cytoplasm around 8 hours p.i. can be confirmed rendering a causative role of lysosomal hydrolases in the pathogenesis of the observed plasma membrane permeability changes possible but not proving it.

摘要

用兔痘病毒感染HeLa细胞单层培养物会导致细胞相关蛋白以及乳酸脱氢酶、酸性磷酸酶和β-葡萄糖醛酸酶的活性显著降低。这种效应在感染后约10小时开始出现,并伴随着培养基中这些酶活性的相应升高。只有少数细胞从感染的单层细胞上脱离,而这些细胞并不能解释蛋白质的释放。病毒粒子的释放可在4℃下被抑制,而蛋白质释放则不能,因此这些事件似乎不是由共同机制引起的。此外,用[14C] - 蔗糖进行的穿透研究表明,蛋白质释放反映了质膜通透性的真正增加。使用酸性磷酸酶的Gomori染色法,可以证实该酶在感染后约8小时释放到细胞质中,这使得溶酶体水解酶在观察到的质膜通透性变化的发病机制中可能起因果作用,但不能证明这一点。

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