Fipronil exposure alters oxidative stress responses of Nile tilapia (Oreochromis niloticus) to acute moderate hypoxia
Main Author: | |
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Publication Date: | 2025 |
Other Authors: | , , |
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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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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1834482614877028352 |