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Differential patterns of reactive oxygen species and antioxidative mechanisms during atrazine injury and sucrose-induced tolerance in Arabidopsis thaliana plantlets

BACKGROUND: Besides being essential for plant structure and metabolism, soluble carbohydrates play important roles in stress responses. Sucrose has been shown to confer to Arabidopsis seedlings a high level of tolerance to the herbicide atrazine, which causes reactive oxygen species (ROS) production...

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Autores principales: Ramel, Fanny, Sulmon, Cécile, Bogard, Matthieu, Couée, Ivan, Gouesbet, Gwenola
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661893/
https://www.ncbi.nlm.nih.gov/pubmed/19284649
http://dx.doi.org/10.1186/1471-2229-9-28
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author Ramel, Fanny
Sulmon, Cécile
Bogard, Matthieu
Couée, Ivan
Gouesbet, Gwenola
author_facet Ramel, Fanny
Sulmon, Cécile
Bogard, Matthieu
Couée, Ivan
Gouesbet, Gwenola
author_sort Ramel, Fanny
collection PubMed
description BACKGROUND: Besides being essential for plant structure and metabolism, soluble carbohydrates play important roles in stress responses. Sucrose has been shown to confer to Arabidopsis seedlings a high level of tolerance to the herbicide atrazine, which causes reactive oxygen species (ROS) production and oxidative stress. The effects of atrazine and of exogenous sucrose on ROS patterns and ROS-scavenging systems were studied. Simultaneous analysis of ROS contents, expression of ROS-related genes and activities of ROS-scavenging enzymes gave an integrative view of physiological state and detoxifying potential under conditions of sensitivity or tolerance. RESULTS: Toxicity of atrazine could be related to inefficient activation of singlet oxygen ((1)O(2)) quenching pathways leading to (1)O(2 )accumulation. Atrazine treatment also increased hydrogen peroxide (H(2)O(2)) content, while reducing gene expressions and enzymatic activities related to two major H(2)O(2)-detoxification pathways. Conversely, sucrose-protected plantlets in the presence of atrazine exhibited efficient (1)O(2 )quenching, low (1)O(2 )accumulation and active H(2)O(2)-detoxifying systems. CONCLUSION: In conclusion, sucrose protection was in part due to activation of specific ROS scavenging systems with consequent reduction of oxidative damages. Importance of ROS combination and potential interferences of sucrose, xenobiotic and ROS signalling pathways are discussed.
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spelling pubmed-26618932009-03-28 Differential patterns of reactive oxygen species and antioxidative mechanisms during atrazine injury and sucrose-induced tolerance in Arabidopsis thaliana plantlets Ramel, Fanny Sulmon, Cécile Bogard, Matthieu Couée, Ivan Gouesbet, Gwenola BMC Plant Biol Research Article BACKGROUND: Besides being essential for plant structure and metabolism, soluble carbohydrates play important roles in stress responses. Sucrose has been shown to confer to Arabidopsis seedlings a high level of tolerance to the herbicide atrazine, which causes reactive oxygen species (ROS) production and oxidative stress. The effects of atrazine and of exogenous sucrose on ROS patterns and ROS-scavenging systems were studied. Simultaneous analysis of ROS contents, expression of ROS-related genes and activities of ROS-scavenging enzymes gave an integrative view of physiological state and detoxifying potential under conditions of sensitivity or tolerance. RESULTS: Toxicity of atrazine could be related to inefficient activation of singlet oxygen ((1)O(2)) quenching pathways leading to (1)O(2 )accumulation. Atrazine treatment also increased hydrogen peroxide (H(2)O(2)) content, while reducing gene expressions and enzymatic activities related to two major H(2)O(2)-detoxification pathways. Conversely, sucrose-protected plantlets in the presence of atrazine exhibited efficient (1)O(2 )quenching, low (1)O(2 )accumulation and active H(2)O(2)-detoxifying systems. CONCLUSION: In conclusion, sucrose protection was in part due to activation of specific ROS scavenging systems with consequent reduction of oxidative damages. Importance of ROS combination and potential interferences of sucrose, xenobiotic and ROS signalling pathways are discussed. BioMed Central 2009-03-13 /pmc/articles/PMC2661893/ /pubmed/19284649 http://dx.doi.org/10.1186/1471-2229-9-28 Text en Copyright © 2009 Ramel et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Ramel, Fanny
Sulmon, Cécile
Bogard, Matthieu
Couée, Ivan
Gouesbet, Gwenola
Differential patterns of reactive oxygen species and antioxidative mechanisms during atrazine injury and sucrose-induced tolerance in Arabidopsis thaliana plantlets
title Differential patterns of reactive oxygen species and antioxidative mechanisms during atrazine injury and sucrose-induced tolerance in Arabidopsis thaliana plantlets
title_full Differential patterns of reactive oxygen species and antioxidative mechanisms during atrazine injury and sucrose-induced tolerance in Arabidopsis thaliana plantlets
title_fullStr Differential patterns of reactive oxygen species and antioxidative mechanisms during atrazine injury and sucrose-induced tolerance in Arabidopsis thaliana plantlets
title_full_unstemmed Differential patterns of reactive oxygen species and antioxidative mechanisms during atrazine injury and sucrose-induced tolerance in Arabidopsis thaliana plantlets
title_short Differential patterns of reactive oxygen species and antioxidative mechanisms during atrazine injury and sucrose-induced tolerance in Arabidopsis thaliana plantlets
title_sort differential patterns of reactive oxygen species and antioxidative mechanisms during atrazine injury and sucrose-induced tolerance in arabidopsis thaliana plantlets
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661893/
https://www.ncbi.nlm.nih.gov/pubmed/19284649
http://dx.doi.org/10.1186/1471-2229-9-28
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