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3-亚甲基氧化吲哚的抗病毒作用机制。

Mechanism of the antiviral action of 3-methyleneoxindole.

作者信息

Tuli V

出版信息

Antimicrob Agents Chemother. 1974 May;5(5):485-91. doi: 10.1128/AAC.5.5.485.

Abstract

The biochemical basis underlying the antiviral action of 3-methyleneoxindole (MO), a plant metabolite, was examined in HeLa cells infected with poliovirus. In the presence of antiviral concentrations of MO, poliovirus-specific ribonucleic acid (RNA) synthesis can proceed normally, and the RNA synthesized under such conditions is infectious. It is suggested that the ability of MO to bind to ribosomes of HeLa cells may underlie the antiviral affect. Data are presented which indicate that poliovirus messenger RNA cannot attach to those ribosomes which already are bound to MO. Consequently, virus-specific polysomes cannot be recovered from infected cells treated with antiviral concentrations of MO. In contrast, antiviral concentrations of MO do not prevent the formation of polysomes in uninfected HeLa cells.

摘要

在感染脊髓灰质炎病毒的HeLa细胞中,研究了植物代谢产物3-亚甲基氧化吲哚(MO)抗病毒作用的生化基础。在抗病毒浓度的MO存在下,脊髓灰质炎病毒特异性核糖核酸(RNA)合成可正常进行,且在此条件下合成的RNA具有感染性。有人提出,MO与HeLa细胞核糖体结合的能力可能是其抗病毒作用的基础。所提供的数据表明,脊髓灰质炎病毒信使RNA无法附着于已与MO结合的那些核糖体。因此,在用抗病毒浓度的MO处理的感染细胞中无法回收病毒特异性多核糖体。相比之下,抗病毒浓度的MO不会阻止未感染的HeLa细胞中多核糖体的形成。

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本文引用的文献

2
Enzymatic dehydration of 3-hydroxymethyloxindole.3-羟甲基氧吲哚的酶促脱水。
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