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埃氏腹水瘤细胞感染脑心肌炎病毒后细胞内能量和离子条件的改变及其对感染中期蛋白质合成的影响。

Alteration of the intracellular energetic and ionic conditions by mengovirus infection of Ehrlich ascites tumor cells and its influence on protein synthesis in the midphase of infection.

作者信息

Egberts E, Hackett P B, Traub P

出版信息

J Virol. 1977 Jun;22(3):591-7. doi: 10.1128/JVI.22.3.591-597.1977.

Abstract

Mengovirus infection of Ehrlich ascites tumor cells caused a change of the intracellular ATP concentration. It increased by 35% within the first 3 h postinfection and then declined to zero within the next 5 h. The decrease in the ATP concentration was due, at least in part, to leakage of ATP into the medium, where it could be demonstrated by the luciferin-luciferase assay. Gross leakage of ATP was observed at 4.5 h postinfection, concomitant with the production of the first intracellular, infectious virus particles. A similar concentration decrease was detected for Mg(2+), the polyamines, and K(+), whereas an increase in the Na(+) concentration was observed. The intracellular Mg(2+) concentration varied synchronously with the ATP level, rising by 16% during the first 3 h postinfection and then progressively falling to lower values in the late period of the infectious cycle. After an initial slight enhancement, the putrescine, spermidine, and spermine concentrations declined at about 1.5 h postinfection. Wherease the intracellular K(+) concentration increased by 17% during the first hour postinfection, the Na(+) concentration diminished by the same value within the same time period, leaving the internal ionic strength unchanged early in infection. Three hours after the beginning of virus infection, there was a rapid decline of K(+) and enhancement of Na(+) within the cell. These alterations of the intracellular energetic and ionic conditions seem to be, at least in part, responsible for the cessation of virus-specific protein synthesis in mengovirus-infected Ehrlich ascites tumor cells commencing 3 to 3.5 h postinfection.

摘要

脑心肌炎病毒感染艾氏腹水瘤细胞会导致细胞内ATP浓度发生变化。感染后最初3小时内,ATP浓度增加了35%,随后在接下来的5小时内降至零。ATP浓度的降低至少部分是由于ATP泄漏到培养基中,通过荧光素-荧光素酶测定法可以在培养基中检测到ATP。在感染后4.5小时观察到ATP大量泄漏,同时伴随着第一批细胞内感染性病毒颗粒的产生。对于Mg(2+)、多胺和K(+)也检测到了类似的浓度降低,而Na(+)浓度则升高。细胞内Mg(2+)浓度与ATP水平同步变化,在感染后最初3小时内上升16%,然后在感染周期后期逐渐降至较低值。在最初略有增加后,腐胺、亚精胺和精胺的浓度在感染后约1.5小时下降。虽然细胞内K(+)浓度在感染后第一小时内增加了17%,但Na(+)浓度在同一时间段内下降了相同的值,使得感染早期细胞内离子强度保持不变。病毒感染开始3小时后,细胞内K(+)迅速下降,Na(+)增加。细胞内能量和离子条件的这些变化似乎至少部分导致了感染脑心肌炎病毒的艾氏腹水瘤细胞在感染后3至3.5小时开始停止病毒特异性蛋白质合成。

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