Fipronil exposure alters oxidative stress responses of Nile tilapia (Oreochromis niloticus) to acute moderate hypoxia

Bibliographic Details
Main Author: Dourado, Priscila Leocádia Rosa [UNESP]
Publication Date: 2025
Other Authors: da Silva, Danilo Grunig Humberto, Alves, Thiago Caique, de Almeida, Eduardo Alves
Format: Article
Language: eng
Source: Repositório Institucional da UNESP
Download full: http://dx.doi.org/10.1016/j.aquatox.2024.107163
https://hdl.handle.net/11449/309121
Summary: Acute hypoxia is known to increase the generation of reactive oxygen species (ROS), leading to modulation in antioxidant defenses. Pollutant exposure can potentiate ROS generation during hypoxic events and impair antioxidant defenses, increasing the susceptibility of hypoxia-tolerant fishes, such as the Nile tilapia (Oreochromis niloticus), to oxidative stress. The purpose of this study was to evaluate oxidative stress responses of O. niloticus to acute (3 and 8 h) moderate hypoxia (dissolved oxygen ≤2 mg/L−1) and how these responses are affected by simultaneous exposure to the insecticide fipronil (0.1 and 0.5 µg L−1). Hypoxia exposure for 3 h caused an increase in glutathione peroxidase (GPx) activity in the gill and also increased catalase (CAT) and glutathione S-transferase (GST) activities in the liver. After 8 h of hypoxia, glutathione reductase (GR) activity increased. DNA damage (comet assay) in erythrocytes was reduced by hypoxia after 3 and 8 h. Fipronil exposure for 3 h decreased CAT activity in the gill, both under normoxia and hypoxia. After 8 h, the combination of fipronil and hypoxia increased GR activity in the gill. In the liver, fipronil exposure under hypoxia for 3 h increased CAT and GR activities; after 8 h, CAT was decreased, and GST increased. GR was also increased by fipronil under normoxia for 8 h. All treatments reduced lipid peroxidation levels in the gills, but in the liver, lipid peroxidation was increased by fipronil after 3 h under normoxia. Moreover, fipronil exposure under hypoxia for 3 and 8 h increased DNA damage in erythrocytes, while 8 h of fipronil exposure under normoxia decreased it, suggesting the activation of DNA repair mechanisms. Results show that both fipronil and hypoxia exposure significantly modulate the oxidative stress parameters of O. niloticus and that the combination of these factors produces more pronounced effects.
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spelling Fipronil exposure alters oxidative stress responses of Nile tilapia (Oreochromis niloticus) to acute moderate hypoxiaBiomarkersFipronilFishHypoxiaOxidative stressAcute hypoxia is known to increase the generation of reactive oxygen species (ROS), leading to modulation in antioxidant defenses. Pollutant exposure can potentiate ROS generation during hypoxic events and impair antioxidant defenses, increasing the susceptibility of hypoxia-tolerant fishes, such as the Nile tilapia (Oreochromis niloticus), to oxidative stress. The purpose of this study was to evaluate oxidative stress responses of O. niloticus to acute (3 and 8 h) moderate hypoxia (dissolved oxygen ≤2 mg/L−1) and how these responses are affected by simultaneous exposure to the insecticide fipronil (0.1 and 0.5 µg L−1). Hypoxia exposure for 3 h caused an increase in glutathione peroxidase (GPx) activity in the gill and also increased catalase (CAT) and glutathione S-transferase (GST) activities in the liver. After 8 h of hypoxia, glutathione reductase (GR) activity increased. DNA damage (comet assay) in erythrocytes was reduced by hypoxia after 3 and 8 h. Fipronil exposure for 3 h decreased CAT activity in the gill, both under normoxia and hypoxia. After 8 h, the combination of fipronil and hypoxia increased GR activity in the gill. In the liver, fipronil exposure under hypoxia for 3 h increased CAT and GR activities; after 8 h, CAT was decreased, and GST increased. GR was also increased by fipronil under normoxia for 8 h. All treatments reduced lipid peroxidation levels in the gills, but in the liver, lipid peroxidation was increased by fipronil after 3 h under normoxia. Moreover, fipronil exposure under hypoxia for 3 and 8 h increased DNA damage in erythrocytes, while 8 h of fipronil exposure under normoxia decreased it, suggesting the activation of DNA repair mechanisms. Results show that both fipronil and hypoxia exposure significantly modulate the oxidative stress parameters of O. niloticus and that the combination of these factors produces more pronounced effects.UNESP – Universidade Estadual Paulista Departamento de Química e Ciências AmbientaisUniversidade Federal de Mato Grosso do Sul, Câmpus de Três Lagoas, Três Lagoas, Mato Grosso do SulFURB Fundação Universidade Regional de Blumenau Department of Natural Sciences, Santa CatarinaUNESP – Universidade Estadual Paulista Departamento de Química e Ciências AmbientaisUniversidade Estadual Paulista (UNESP)Universidade Federal de Mato Grosso do Sul (UFMS)FURB Fundação Universidade Regional de BlumenauDourado, Priscila Leocádia Rosa [UNESP]da Silva, Danilo Grunig HumbertoAlves, Thiago Caiquede Almeida, Eduardo Alves2025-04-29T20:14:26Z2025-01-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://dx.doi.org/10.1016/j.aquatox.2024.107163Aquatic Toxicology, v. 278.1879-15140166-445Xhttps://hdl.handle.net/11449/30912110.1016/j.aquatox.2024.1071632-s2.0-85209649524Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengAquatic Toxicologyinfo:eu-repo/semantics/openAccess2025-04-30T13:36:18Zoai:repositorio.unesp.br:11449/309121Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestrepositoriounesp@unesp.bropendoar:29462025-04-30T13:36:18Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Fipronil exposure alters oxidative stress responses of Nile tilapia (Oreochromis niloticus) to acute moderate hypoxia
title Fipronil exposure alters oxidative stress responses of Nile tilapia (Oreochromis niloticus) to acute moderate hypoxia
spellingShingle Fipronil exposure alters oxidative stress responses of Nile tilapia (Oreochromis niloticus) to acute moderate hypoxia
Dourado, Priscila Leocádia Rosa [UNESP]
Biomarkers
Fipronil
Fish
Hypoxia
Oxidative stress
title_short Fipronil exposure alters oxidative stress responses of Nile tilapia (Oreochromis niloticus) to acute moderate hypoxia
title_full Fipronil exposure alters oxidative stress responses of Nile tilapia (Oreochromis niloticus) to acute moderate hypoxia
title_fullStr Fipronil exposure alters oxidative stress responses of Nile tilapia (Oreochromis niloticus) to acute moderate hypoxia
title_full_unstemmed Fipronil exposure alters oxidative stress responses of Nile tilapia (Oreochromis niloticus) to acute moderate hypoxia
title_sort Fipronil exposure alters oxidative stress responses of Nile tilapia (Oreochromis niloticus) to acute moderate hypoxia
author Dourado, Priscila Leocádia Rosa [UNESP]
author_facet Dourado, Priscila Leocádia Rosa [UNESP]
da Silva, Danilo Grunig Humberto
Alves, Thiago Caique
de Almeida, Eduardo Alves
author_role author
author2 da Silva, Danilo Grunig Humberto
Alves, Thiago Caique
de Almeida, Eduardo Alves
author2_role author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (UNESP)
Universidade Federal de Mato Grosso do Sul (UFMS)
FURB Fundação Universidade Regional de Blumenau
dc.contributor.author.fl_str_mv Dourado, Priscila Leocádia Rosa [UNESP]
da Silva, Danilo Grunig Humberto
Alves, Thiago Caique
de Almeida, Eduardo Alves
dc.subject.por.fl_str_mv Biomarkers
Fipronil
Fish
Hypoxia
Oxidative stress
topic Biomarkers
Fipronil
Fish
Hypoxia
Oxidative stress
description Acute hypoxia is known to increase the generation of reactive oxygen species (ROS), leading to modulation in antioxidant defenses. Pollutant exposure can potentiate ROS generation during hypoxic events and impair antioxidant defenses, increasing the susceptibility of hypoxia-tolerant fishes, such as the Nile tilapia (Oreochromis niloticus), to oxidative stress. The purpose of this study was to evaluate oxidative stress responses of O. niloticus to acute (3 and 8 h) moderate hypoxia (dissolved oxygen ≤2 mg/L−1) and how these responses are affected by simultaneous exposure to the insecticide fipronil (0.1 and 0.5 µg L−1). Hypoxia exposure for 3 h caused an increase in glutathione peroxidase (GPx) activity in the gill and also increased catalase (CAT) and glutathione S-transferase (GST) activities in the liver. After 8 h of hypoxia, glutathione reductase (GR) activity increased. DNA damage (comet assay) in erythrocytes was reduced by hypoxia after 3 and 8 h. Fipronil exposure for 3 h decreased CAT activity in the gill, both under normoxia and hypoxia. After 8 h, the combination of fipronil and hypoxia increased GR activity in the gill. In the liver, fipronil exposure under hypoxia for 3 h increased CAT and GR activities; after 8 h, CAT was decreased, and GST increased. GR was also increased by fipronil under normoxia for 8 h. All treatments reduced lipid peroxidation levels in the gills, but in the liver, lipid peroxidation was increased by fipronil after 3 h under normoxia. Moreover, fipronil exposure under hypoxia for 3 and 8 h increased DNA damage in erythrocytes, while 8 h of fipronil exposure under normoxia decreased it, suggesting the activation of DNA repair mechanisms. Results show that both fipronil and hypoxia exposure significantly modulate the oxidative stress parameters of O. niloticus and that the combination of these factors produces more pronounced effects.
publishDate 2025
dc.date.none.fl_str_mv 2025-04-29T20:14:26Z
2025-01-01
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1016/j.aquatox.2024.107163
Aquatic Toxicology, v. 278.
1879-1514
0166-445X
https://hdl.handle.net/11449/309121
10.1016/j.aquatox.2024.107163
2-s2.0-85209649524
url http://dx.doi.org/10.1016/j.aquatox.2024.107163
https://hdl.handle.net/11449/309121
identifier_str_mv Aquatic Toxicology, v. 278.
1879-1514
0166-445X
10.1016/j.aquatox.2024.107163
2-s2.0-85209649524
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Aquatic Toxicology
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.source.none.fl_str_mv Scopus
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
repository.mail.fl_str_mv repositoriounesp@unesp.br
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