Oxidative stress in Vero cells infected with vesicular stomatitis virus
Viral-induced apoptosis might be mediated by oxidative stress. It has already been described that cell death in vesicular stomatitis virus (VSV)-infected cells occurs by apoptosis. In this study, oxidative stress parameters present in VSV-infected Vero cells were analyzed. Lipid peroxides (LP) were...
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2006
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Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03005526_v49_n5_p294_Riva http://hdl.handle.net/20.500.12110/paper_03005526_v49_n5_p294_Riva |
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paper:paper_03005526_v49_n5_p294_Riva2023-06-08T15:27:20Z Oxidative stress in Vero cells infected with vesicular stomatitis virus Lipid peroxidation Superoxide dismutase Vesicular stomatitis virus antioxidant caspase 3 cell protein guaiacol superoxide dismutase animal cell apoptosis article cell death cell viability enzyme activity genetic susceptibility lipid peroxidation nonhuman oxidative stress priority journal protein degradation protein lipid interaction Vero cell Vesicular stomatitis virus virus infection Animals Cercopithecus aethiops Lipid Peroxides Oxidative Stress Rhabdoviridae Infections Superoxide Dismutase Time Factors Vero Cells Vesicular stomatitis-Indiana virus Vesicular stomatitis virus Viral-induced apoptosis might be mediated by oxidative stress. It has already been described that cell death in vesicular stomatitis virus (VSV)-infected cells occurs by apoptosis. In this study, oxidative stress parameters present in VSV-infected Vero cells were analyzed. Lipid peroxides (LP) were evaluated in cellular extracts and expressed as thiobarbituric acid-reactive substances. LP levels exhibited a rise at different times post infection, according to the multiplicity of infection (MOI), while the presence of cycloheximide determined a reduction on LP. Also, an increase in protein degradation products and a decrease in polyunsaturated fatty acids content was observed, indicating that cellular proteins and lipids began to be susceptible to degradation during VSV infection. In addition, we analyzed cell viability of VSV-infected Vero cells, which were incubated in the presence of butylated hydroxyanisole. This antioxidant was able to protect Vero cells, at least at MOIs assayed in this study, and to reduce viral yield only when VSV infection was done at MOI 0.05. Further, superoxide dismutases, which occupy the first step within the antioxidant enzyme cascade, also exhibit a rise in VSV-infected Vero cells, at different MOI. These results suggest that both an oxidative stress and an antioxidative cell response precede the induction of apoptosis by VSV. Copyright © 2006 S. Karger AG. 2006 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03005526_v49_n5_p294_Riva http://hdl.handle.net/20.500.12110/paper_03005526_v49_n5_p294_Riva |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-134 |
collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
topic |
Lipid peroxidation Superoxide dismutase Vesicular stomatitis virus antioxidant caspase 3 cell protein guaiacol superoxide dismutase animal cell apoptosis article cell death cell viability enzyme activity genetic susceptibility lipid peroxidation nonhuman oxidative stress priority journal protein degradation protein lipid interaction Vero cell Vesicular stomatitis virus virus infection Animals Cercopithecus aethiops Lipid Peroxides Oxidative Stress Rhabdoviridae Infections Superoxide Dismutase Time Factors Vero Cells Vesicular stomatitis-Indiana virus Vesicular stomatitis virus |
spellingShingle |
Lipid peroxidation Superoxide dismutase Vesicular stomatitis virus antioxidant caspase 3 cell protein guaiacol superoxide dismutase animal cell apoptosis article cell death cell viability enzyme activity genetic susceptibility lipid peroxidation nonhuman oxidative stress priority journal protein degradation protein lipid interaction Vero cell Vesicular stomatitis virus virus infection Animals Cercopithecus aethiops Lipid Peroxides Oxidative Stress Rhabdoviridae Infections Superoxide Dismutase Time Factors Vero Cells Vesicular stomatitis-Indiana virus Vesicular stomatitis virus Oxidative stress in Vero cells infected with vesicular stomatitis virus |
topic_facet |
Lipid peroxidation Superoxide dismutase Vesicular stomatitis virus antioxidant caspase 3 cell protein guaiacol superoxide dismutase animal cell apoptosis article cell death cell viability enzyme activity genetic susceptibility lipid peroxidation nonhuman oxidative stress priority journal protein degradation protein lipid interaction Vero cell Vesicular stomatitis virus virus infection Animals Cercopithecus aethiops Lipid Peroxides Oxidative Stress Rhabdoviridae Infections Superoxide Dismutase Time Factors Vero Cells Vesicular stomatitis-Indiana virus Vesicular stomatitis virus |
description |
Viral-induced apoptosis might be mediated by oxidative stress. It has already been described that cell death in vesicular stomatitis virus (VSV)-infected cells occurs by apoptosis. In this study, oxidative stress parameters present in VSV-infected Vero cells were analyzed. Lipid peroxides (LP) were evaluated in cellular extracts and expressed as thiobarbituric acid-reactive substances. LP levels exhibited a rise at different times post infection, according to the multiplicity of infection (MOI), while the presence of cycloheximide determined a reduction on LP. Also, an increase in protein degradation products and a decrease in polyunsaturated fatty acids content was observed, indicating that cellular proteins and lipids began to be susceptible to degradation during VSV infection. In addition, we analyzed cell viability of VSV-infected Vero cells, which were incubated in the presence of butylated hydroxyanisole. This antioxidant was able to protect Vero cells, at least at MOIs assayed in this study, and to reduce viral yield only when VSV infection was done at MOI 0.05. Further, superoxide dismutases, which occupy the first step within the antioxidant enzyme cascade, also exhibit a rise in VSV-infected Vero cells, at different MOI. These results suggest that both an oxidative stress and an antioxidative cell response precede the induction of apoptosis by VSV. Copyright © 2006 S. Karger AG. |
title |
Oxidative stress in Vero cells infected with vesicular stomatitis virus |
title_short |
Oxidative stress in Vero cells infected with vesicular stomatitis virus |
title_full |
Oxidative stress in Vero cells infected with vesicular stomatitis virus |
title_fullStr |
Oxidative stress in Vero cells infected with vesicular stomatitis virus |
title_full_unstemmed |
Oxidative stress in Vero cells infected with vesicular stomatitis virus |
title_sort |
oxidative stress in vero cells infected with vesicular stomatitis virus |
publishDate |
2006 |
url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03005526_v49_n5_p294_Riva http://hdl.handle.net/20.500.12110/paper_03005526_v49_n5_p294_Riva |
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1768544818661687296 |