Viral infection of Emiliania huxleyi (Prymnesiophyceae) leads to elevated production of reactive oxygen species

Viral infection of Emiliania huxleyi (Prymnesiophyceae) leads to elevated production of reactive oxygen species
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DOI:
10.1111/j.1529-8817.2006.00256.x
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发表时间:
2006-10-01
影响因子:
2.9
通讯作者:
Wilson, William H.
Wilson, William H.
中科院分区:
生物学3区
文献类型:
--
作者:
Evans, Claire;Malin, Gillian;Wilson, William H.

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研究了病毒侵染虎纹夜蛾(Emily huxleyi(Lohman)Hay)和莫勒(Mohler)对细胞内活性氧(ROS)浓度、过氧化氢(H_2O_2)分泌和细胞光合作用能力(CPC)的影响。在病毒诱导的E.huxleyi培养崩溃期间,细胞内ROS浓度普遍升高,达到非感染对照培养的两倍左右。受感染的培养液中的过氧化氢浓度也从大约130 nM的本底水平增加到大约580 nM,而对照组的水平下降。这些数据表明,受感染的细胞中的氧化应激水平升高。虽然ROS产生的确切机制尚未确定,但排除了传统防御相关的氧化爆发,因为没有发现加入病毒后ROS在细胞内快速积累的证据。在感染的文化中CPC大幅下降,从健康的0.6-0任意单位。显然,感染扰乱了正常的光合作用过程,这可能通过中断PSII水平的电子传输链来导致ROS的产生。另外,ROS也可能是虎纹埃希菌病毒复制所必需的,这可能是由于与病毒诱导的细胞死亡或与一般死亡过程有关。
The effect of viral infection of Emiliania huxleyi (Lohman) Hay and Mohler on the concentration of intracellular reactive oxygen species (ROS), hydrogen peroxide (H2O2) excretion and cell photosynthetic capacity (CPC) was examined. During the crash of an E. huxleyi culture induced by viruses intracellular ROS concentrations were generally elevated and reached levels of approximately double those observed in non-infected control cultures. H2O2 concentrations also increased in the media of the infected cultures from background levels of around 130 nM to approximately 580 nM while levels in the controls decreased. These data suggest that oxidative stress is elevated in infected cells. Although the precise mechanism for ROS production was not identified, a traditional defense related oxidative burst was ruled out, as no evidence of a rapid intracellular accumulation of ROS following addition of the virus was found. CPC declined substantially in the infected culture from a healthy 0.6-0 arbitrary units. Clearly infection disrupted normal photosynthetic processes, which could lead to the production of ROS via interruption of the electron transport chain at the PSII level. Alternatively, ROS may also be a necessary requirement for viral replication in E. huxleyi, possibly due to a link with viral-induced cell death or associated with general death processes.