Effects of imidacloprid on viability and increase of reactive oxygen and nitrogen species in HepG2 cell line
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1080/15376516.2021.1992553 http://hdl.handle.net/11449/233760 |
Resumo: | Imidacloprid (IMD) is a neonicotinoid insecticide used in large quantities worldwide in both veterinary and agronomic applications. Several studies have shown adverse effects of IMD on non-target organisms, with the liver being identified as the main affected organ. This study aimed to evaluate the effects of IMD on human hepatoblastoma (HepG2) cells. HepG2 were exposed to IMD (0.25–2.0 mM) for 24 and 48 h. IMD treatment resulted in cytotoxicity in the HepG2, inhibiting cell proliferation in a dose- and time-dependent manner, starting at concentrations of 0.5 mM (24 h) and 0.25 mM (48 h), and reducing cell viability from 0.5 mM onwards (24 and 48 h). IMD significantly decreased the mitochondrial membrane potential at both time points investigated (2.0 mM), and also induced damage to the cell membrane, demonstrated by significant dose and time-dependent increases in lactate dehydrogenase (LDH) release from concentrations of 1.0 mM (24 h) and 0.5 mM (48 h) upwards. IMD treatment also increased the production of reactive oxygen and nitrogen species (ROS/RNS) at rates above 50% following 0.5 mM (24 h) or 0.25 mM (48 h) concentrations, and caused a significant decrease in reduced/oxidized glutathione ratio (GSH/GSSG), indicating oxidative stress. Furthermore, the antioxidant dithiothreitol, which reacts with ROS/RNS and acts as a thiol reducing agent, inhibited the cytotoxic effect of IMD. In addition, the metabolite IMD-olefin was more toxic than IMD. Our results indicate that IMD induces cytotoxicity in HepG2 cells and that this effect may be associated with an increase in the generation of ROS/RNS. |
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Effects of imidacloprid on viability and increase of reactive oxygen and nitrogen species in HepG2 cell linecell deathCytotoxicityinsecticideliveroxidative stressImidacloprid (IMD) is a neonicotinoid insecticide used in large quantities worldwide in both veterinary and agronomic applications. Several studies have shown adverse effects of IMD on non-target organisms, with the liver being identified as the main affected organ. This study aimed to evaluate the effects of IMD on human hepatoblastoma (HepG2) cells. HepG2 were exposed to IMD (0.25–2.0 mM) for 24 and 48 h. IMD treatment resulted in cytotoxicity in the HepG2, inhibiting cell proliferation in a dose- and time-dependent manner, starting at concentrations of 0.5 mM (24 h) and 0.25 mM (48 h), and reducing cell viability from 0.5 mM onwards (24 and 48 h). IMD significantly decreased the mitochondrial membrane potential at both time points investigated (2.0 mM), and also induced damage to the cell membrane, demonstrated by significant dose and time-dependent increases in lactate dehydrogenase (LDH) release from concentrations of 1.0 mM (24 h) and 0.5 mM (48 h) upwards. IMD treatment also increased the production of reactive oxygen and nitrogen species (ROS/RNS) at rates above 50% following 0.5 mM (24 h) or 0.25 mM (48 h) concentrations, and caused a significant decrease in reduced/oxidized glutathione ratio (GSH/GSSG), indicating oxidative stress. Furthermore, the antioxidant dithiothreitol, which reacts with ROS/RNS and acts as a thiol reducing agent, inhibited the cytotoxic effect of IMD. In addition, the metabolite IMD-olefin was more toxic than IMD. Our results indicate that IMD induces cytotoxicity in HepG2 cells and that this effect may be associated with an increase in the generation of ROS/RNS.Department of Animal Science College of Agricultural and Technological Sciences São Paulo State University (UNESP)Department of Biochemistry Maringá State University (UEM)Department of Animal Science College of Agricultural and Technological Sciences São Paulo State University (UNESP)Universidade Estadual Paulista (UNESP)Universidade Estadual de Maringá (UEM)Guimarães, Anilda Rufino de Jesus Santos [UNESP]Bizerra, Paulo Francisco Veiga [UNESP]Miranda, Camila Araújo [UNESP]Mingatto, Fábio Erminio [UNESP]2022-05-01T10:02:57Z2022-05-01T10:02:57Z2022-01-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article204-212http://dx.doi.org/10.1080/15376516.2021.1992553Toxicology Mechanisms and Methods, v. 32, n. 3, p. 204-212, 2022.1537-65241537-6516http://hdl.handle.net/11449/23376010.1080/15376516.2021.19925532-s2.0-85118233622Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengToxicology Mechanisms and Methodsinfo:eu-repo/semantics/openAccess2024-05-07T13:48:05Zoai:repositorio.unesp.br:11449/233760Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T22:17:01.465564Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Effects of imidacloprid on viability and increase of reactive oxygen and nitrogen species in HepG2 cell line |
title |
Effects of imidacloprid on viability and increase of reactive oxygen and nitrogen species in HepG2 cell line |
spellingShingle |
Effects of imidacloprid on viability and increase of reactive oxygen and nitrogen species in HepG2 cell line Guimarães, Anilda Rufino de Jesus Santos [UNESP] cell death Cytotoxicity insecticide liver oxidative stress |
title_short |
Effects of imidacloprid on viability and increase of reactive oxygen and nitrogen species in HepG2 cell line |
title_full |
Effects of imidacloprid on viability and increase of reactive oxygen and nitrogen species in HepG2 cell line |
title_fullStr |
Effects of imidacloprid on viability and increase of reactive oxygen and nitrogen species in HepG2 cell line |
title_full_unstemmed |
Effects of imidacloprid on viability and increase of reactive oxygen and nitrogen species in HepG2 cell line |
title_sort |
Effects of imidacloprid on viability and increase of reactive oxygen and nitrogen species in HepG2 cell line |
author |
Guimarães, Anilda Rufino de Jesus Santos [UNESP] |
author_facet |
Guimarães, Anilda Rufino de Jesus Santos [UNESP] Bizerra, Paulo Francisco Veiga [UNESP] Miranda, Camila Araújo [UNESP] Mingatto, Fábio Erminio [UNESP] |
author_role |
author |
author2 |
Bizerra, Paulo Francisco Veiga [UNESP] Miranda, Camila Araújo [UNESP] Mingatto, Fábio Erminio [UNESP] |
author2_role |
author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual Paulista (UNESP) Universidade Estadual de Maringá (UEM) |
dc.contributor.author.fl_str_mv |
Guimarães, Anilda Rufino de Jesus Santos [UNESP] Bizerra, Paulo Francisco Veiga [UNESP] Miranda, Camila Araújo [UNESP] Mingatto, Fábio Erminio [UNESP] |
dc.subject.por.fl_str_mv |
cell death Cytotoxicity insecticide liver oxidative stress |
topic |
cell death Cytotoxicity insecticide liver oxidative stress |
description |
Imidacloprid (IMD) is a neonicotinoid insecticide used in large quantities worldwide in both veterinary and agronomic applications. Several studies have shown adverse effects of IMD on non-target organisms, with the liver being identified as the main affected organ. This study aimed to evaluate the effects of IMD on human hepatoblastoma (HepG2) cells. HepG2 were exposed to IMD (0.25–2.0 mM) for 24 and 48 h. IMD treatment resulted in cytotoxicity in the HepG2, inhibiting cell proliferation in a dose- and time-dependent manner, starting at concentrations of 0.5 mM (24 h) and 0.25 mM (48 h), and reducing cell viability from 0.5 mM onwards (24 and 48 h). IMD significantly decreased the mitochondrial membrane potential at both time points investigated (2.0 mM), and also induced damage to the cell membrane, demonstrated by significant dose and time-dependent increases in lactate dehydrogenase (LDH) release from concentrations of 1.0 mM (24 h) and 0.5 mM (48 h) upwards. IMD treatment also increased the production of reactive oxygen and nitrogen species (ROS/RNS) at rates above 50% following 0.5 mM (24 h) or 0.25 mM (48 h) concentrations, and caused a significant decrease in reduced/oxidized glutathione ratio (GSH/GSSG), indicating oxidative stress. Furthermore, the antioxidant dithiothreitol, which reacts with ROS/RNS and acts as a thiol reducing agent, inhibited the cytotoxic effect of IMD. In addition, the metabolite IMD-olefin was more toxic than IMD. Our results indicate that IMD induces cytotoxicity in HepG2 cells and that this effect may be associated with an increase in the generation of ROS/RNS. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-05-01T10:02:57Z 2022-05-01T10:02:57Z 2022-01-01 |
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/10.1080/15376516.2021.1992553 Toxicology Mechanisms and Methods, v. 32, n. 3, p. 204-212, 2022. 1537-6524 1537-6516 http://hdl.handle.net/11449/233760 10.1080/15376516.2021.1992553 2-s2.0-85118233622 |
url |
http://dx.doi.org/10.1080/15376516.2021.1992553 http://hdl.handle.net/11449/233760 |
identifier_str_mv |
Toxicology Mechanisms and Methods, v. 32, n. 3, p. 204-212, 2022. 1537-6524 1537-6516 10.1080/15376516.2021.1992553 2-s2.0-85118233622 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Toxicology Mechanisms and Methods |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
204-212 |
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 |
|
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1808129413166923776 |