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...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Riva, D.A., Ríos De Molina, M.C., Rocchetta, I., Gerhardt, E., Coulombié, F.C., Mersich, S.E.
Formato: JOUR
Materias:
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_03005526_v49_n5_p294_Riva
Aporte de:
id todo:paper_03005526_v49_n5_p294_Riva
record_format dspace
spelling todo:paper_03005526_v49_n5_p294_Riva2023-10-03T15:17:40Z Oxidative stress in Vero cells infected with vesicular stomatitis virus Riva, D.A. Ríos De Molina, M.C. Rocchetta, I. Gerhardt, E. Coulombié, F.C. Mersich, S.E. 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. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar 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
Riva, D.A.
Ríos De Molina, M.C.
Rocchetta, I.
Gerhardt, E.
Coulombié, F.C.
Mersich, S.E.
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.
format JOUR
author Riva, D.A.
Ríos De Molina, M.C.
Rocchetta, I.
Gerhardt, E.
Coulombié, F.C.
Mersich, S.E.
author_facet Riva, D.A.
Ríos De Molina, M.C.
Rocchetta, I.
Gerhardt, E.
Coulombié, F.C.
Mersich, S.E.
author_sort Riva, D.A.
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
url http://hdl.handle.net/20.500.12110/paper_03005526_v49_n5_p294_Riva
work_keys_str_mv AT rivada oxidativestressinverocellsinfectedwithvesicularstomatitisvirus
AT riosdemolinamc oxidativestressinverocellsinfectedwithvesicularstomatitisvirus
AT rocchettai oxidativestressinverocellsinfectedwithvesicularstomatitisvirus
AT gerhardte oxidativestressinverocellsinfectedwithvesicularstomatitisvirus
AT coulombiefc oxidativestressinverocellsinfectedwithvesicularstomatitisvirus
AT mersichse oxidativestressinverocellsinfectedwithvesicularstomatitisvirus
_version_ 1782027623949402112