Betanodavirus induces oxidative Stress-Mediated cell death that prevented by Anti-Oxidants and zfcatalase in fish cells

Chih Wei Chang, Yu Chin Su, Guor Mour Her, Chuian Fu Ken, Jiann Ruey Hong

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

The role of oxidative stress in the pathogenesis of RNA nervous necrosis virus infection is still unknown. Red-spotted grouper nervous necrosis virus (RGNNV) induced free radical species (ROS) production at 12-24 h post-infection (pi; early replication stage) in fish GF-1 cells, and then at middle replication stage (24-48 h pi), this ROS signal may upregulate some expressions of the anti-oxidant enzymes Cu/Zn SOD and catalase, and eventually expression of the transcription factor Nrf2. Furthermore, both antioxidants diphenyliodonium and N-acetylcysteine or overexpression of zebrafish catalase in GF-1 cells also reduced ROS production and protected cells for enhancing host survival rate due to RGNNV infection. Furthermore, localization of ROS production using esterase activity and Mitotracker staining assays found that the ROS generated can affect mitochondrial morphology changes and causes ΔΨ loss, both of which can be reversed by antioxidant treatment. Taken together, our data suggest that RGNNV induced oxidative stress response for playing dual role that can initiate the host oxidative stress defense system to upregulate expression of antioxidant enzymes and induces cell death via disrupting the mitochondrial morphology and inducing ΔΨ loss, which can be reversed by anti-oxidants and zfcatalase, which provide new insight into betanodavirus-induced ROS-mediated pathogenesis.

Original languageEnglish
Article numbere25853
JournalPLoS ONE
Volume6
Issue number10
DOIs
Publication statusPublished - 2011 Oct 3

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Nodaviridae
Betanodavirus
Oxidative stress
Cell death
Viruses
Oxidants
oxidants
Fish
grouper
cell death
necrosis
Fishes
Oxidative Stress
Cell Death
Necrosis
oxidative stress
viruses
Antioxidants
Virus Diseases
fish

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)
  • General

Cite this

Chang, Chih Wei ; Su, Yu Chin ; Her, Guor Mour ; Ken, Chuian Fu ; Hong, Jiann Ruey. / Betanodavirus induces oxidative Stress-Mediated cell death that prevented by Anti-Oxidants and zfcatalase in fish cells. In: PLoS ONE. 2011 ; Vol. 6, No. 10.
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abstract = "The role of oxidative stress in the pathogenesis of RNA nervous necrosis virus infection is still unknown. Red-spotted grouper nervous necrosis virus (RGNNV) induced free radical species (ROS) production at 12-24 h post-infection (pi; early replication stage) in fish GF-1 cells, and then at middle replication stage (24-48 h pi), this ROS signal may upregulate some expressions of the anti-oxidant enzymes Cu/Zn SOD and catalase, and eventually expression of the transcription factor Nrf2. Furthermore, both antioxidants diphenyliodonium and N-acetylcysteine or overexpression of zebrafish catalase in GF-1 cells also reduced ROS production and protected cells for enhancing host survival rate due to RGNNV infection. Furthermore, localization of ROS production using esterase activity and Mitotracker staining assays found that the ROS generated can affect mitochondrial morphology changes and causes ΔΨ loss, both of which can be reversed by antioxidant treatment. Taken together, our data suggest that RGNNV induced oxidative stress response for playing dual role that can initiate the host oxidative stress defense system to upregulate expression of antioxidant enzymes and induces cell death via disrupting the mitochondrial morphology and inducing ΔΨ loss, which can be reversed by anti-oxidants and zfcatalase, which provide new insight into betanodavirus-induced ROS-mediated pathogenesis.",
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Betanodavirus induces oxidative Stress-Mediated cell death that prevented by Anti-Oxidants and zfcatalase in fish cells. / Chang, Chih Wei; Su, Yu Chin; Her, Guor Mour; Ken, Chuian Fu; Hong, Jiann Ruey.

In: PLoS ONE, Vol. 6, No. 10, e25853, 03.10.2011.

Research output: Contribution to journalArticle

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