Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercury
Main Author: | |
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Publication Date: | 2018 |
Other Authors: | , , , , , |
Format: | Article |
Language: | eng |
Source: | Repositório Institucional da UNESP |
Download full: | http://dx.doi.org/10.1080/01480545.2018.1497045 http://hdl.handle.net/11449/176841 |
Summary: | Humans and animals can be exposed to different chemical forms of mercury (Hg) in the environment. For example, methylmercury (MeHg)-contaminated fish is part of the basic diet of the riparian population in the Brazilian Amazon Basin, which leads to high total blood and plasma Hg levels in people living therein. Hg induces toxic effects mainly through oxidative stress. Different compounds have been used to prevent the damage caused by MeHg-induced reactive oxygen species (ROS). This study aims to investigate the in vivo effects of sub-chronic exposure to low MeHg levels on the mitochondrial oxidative status and to evaluate the niacin protective effect against MeHg-induced oxidative stress. For this purpose, Male Wistar rats were divided into four groups: control group, treated with drinking water on a daily basis; group exposed to MeHg at a dose of 100 µg/kg/day; group that received niacin at a dose of 50 mg/kg/day in drinking water, with drinking water being administered by gavage; group that received niacin at a dose of 50 mg/kg/day in drinking water as well as MeHg at a dose of 100 µg/kg/day. After 12 weeks, the rats, which weighed 500–550 g, were sacrificed, and their liver mitochondria were isolated by standard differential centrifugation. Sub-chronic exposure to MeHg (100 µg/kg/day for 12 weeks) led to mitochondrial swelling (p < 0.05) and induced ROS overproduction as determined by increased DFCH oxidation (p < 0.05), increased gluthatione oxidation (p < 0.05), and reduced protein thiol content (p < 0.05). In contrast, niacin supplementation inhibited oxidative stress, which counteracted and minimized the toxic MeHg effects on mitochondria. |
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Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercuryMethylmercurymitochondrianiacinprotective effectsub-chronicHumans and animals can be exposed to different chemical forms of mercury (Hg) in the environment. For example, methylmercury (MeHg)-contaminated fish is part of the basic diet of the riparian population in the Brazilian Amazon Basin, which leads to high total blood and plasma Hg levels in people living therein. Hg induces toxic effects mainly through oxidative stress. Different compounds have been used to prevent the damage caused by MeHg-induced reactive oxygen species (ROS). This study aims to investigate the in vivo effects of sub-chronic exposure to low MeHg levels on the mitochondrial oxidative status and to evaluate the niacin protective effect against MeHg-induced oxidative stress. For this purpose, Male Wistar rats were divided into four groups: control group, treated with drinking water on a daily basis; group exposed to MeHg at a dose of 100 µg/kg/day; group that received niacin at a dose of 50 mg/kg/day in drinking water, with drinking water being administered by gavage; group that received niacin at a dose of 50 mg/kg/day in drinking water as well as MeHg at a dose of 100 µg/kg/day. After 12 weeks, the rats, which weighed 500–550 g, were sacrificed, and their liver mitochondria were isolated by standard differential centrifugation. Sub-chronic exposure to MeHg (100 µg/kg/day for 12 weeks) led to mitochondrial swelling (p < 0.05) and induced ROS overproduction as determined by increased DFCH oxidation (p < 0.05), increased gluthatione oxidation (p < 0.05), and reduced protein thiol content (p < 0.05). In contrast, niacin supplementation inhibited oxidative stress, which counteracted and minimized the toxic MeHg effects on mitochondria.Faculdade de Ciências Farmacêuticas de Ribeirão Preto Departamento de Análises Clínicas Toxicológicas e Bromatológicas Universidade de São PauloFaculdade de Ciências Agronômicas Departamento de Bioprocessos e Biotecnologia Universidade Estadual PaulistaDepartamento de Patologia Faculdade de Medicina de Botucatu Universidade Estadual Paulista TOXICAM–Núcleo de Avaliação do Impacto Ambiental sobre a Saúde HumanaLaboratório de Pesquisa em Toxicologia Programa de Pós-Graduação em Ciências Farmacêuticas Universidade de SorocabaFaculdade de Filosofia Ciências e Letras de Ribeirão Preto Departamento de Química Universidade de São PauloInstituto Nacional de Tecnologias Alternativas de Detecção Avaliação Toxicológica e Remoção de Micropututantes e Radioativos (INCT-DATREM) Unesp Instituto de QuímicaFaculdade de Ciências Agronômicas Departamento de Bioprocessos e Biotecnologia Universidade Estadual PaulistaDepartamento de Patologia Faculdade de Medicina de Botucatu Universidade Estadual Paulista TOXICAM–Núcleo de Avaliação do Impacto Ambiental sobre a Saúde HumanaInstituto Nacional de Tecnologias Alternativas de Detecção Avaliação Toxicológica e Remoção de Micropututantes e Radioativos (INCT-DATREM) Unesp Instituto de QuímicaUniversidade de São Paulo (USP)Universidade Estadual Paulista (Unesp)Universidade de SorocabaPereira, Lílian Cristina [UNESP]de Paula, Eloisa SilvaPazin, MuriloCarneiro, Maria Fernanda HornosGrotto, DeniseBarbosa, FernandoDorta, Daniel Junqueira [UNESP]2018-12-11T17:22:43Z2018-12-11T17:22:43Z2018-01-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://dx.doi.org/10.1080/01480545.2018.1497045Drug and Chemical Toxicology.1525-60140148-0545http://hdl.handle.net/11449/17684110.1080/01480545.2018.14970452-s2.0-85053294086186557912427276Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengDrug and Chemical Toxicology0,4600,460info:eu-repo/semantics/openAccess2021-10-23T20:11:23Zoai:repositorio.unesp.br:11449/176841Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462021-10-23T20:11:23Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercury |
title |
Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercury |
spellingShingle |
Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercury Pereira, Lílian Cristina [UNESP] Methylmercury mitochondria niacin protective effect sub-chronic |
title_short |
Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercury |
title_full |
Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercury |
title_fullStr |
Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercury |
title_full_unstemmed |
Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercury |
title_sort |
Niacin prevents mitochondrial oxidative stress caused by sub-chronic exposure to methylmercury |
author |
Pereira, Lílian Cristina [UNESP] |
author_facet |
Pereira, Lílian Cristina [UNESP] de Paula, Eloisa Silva Pazin, Murilo Carneiro, Maria Fernanda Hornos Grotto, Denise Barbosa, Fernando Dorta, Daniel Junqueira [UNESP] |
author_role |
author |
author2 |
de Paula, Eloisa Silva Pazin, Murilo Carneiro, Maria Fernanda Hornos Grotto, Denise Barbosa, Fernando Dorta, Daniel Junqueira [UNESP] |
author2_role |
author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade de São Paulo (USP) Universidade Estadual Paulista (Unesp) Universidade de Sorocaba |
dc.contributor.author.fl_str_mv |
Pereira, Lílian Cristina [UNESP] de Paula, Eloisa Silva Pazin, Murilo Carneiro, Maria Fernanda Hornos Grotto, Denise Barbosa, Fernando Dorta, Daniel Junqueira [UNESP] |
dc.subject.por.fl_str_mv |
Methylmercury mitochondria niacin protective effect sub-chronic |
topic |
Methylmercury mitochondria niacin protective effect sub-chronic |
description |
Humans and animals can be exposed to different chemical forms of mercury (Hg) in the environment. For example, methylmercury (MeHg)-contaminated fish is part of the basic diet of the riparian population in the Brazilian Amazon Basin, which leads to high total blood and plasma Hg levels in people living therein. Hg induces toxic effects mainly through oxidative stress. Different compounds have been used to prevent the damage caused by MeHg-induced reactive oxygen species (ROS). This study aims to investigate the in vivo effects of sub-chronic exposure to low MeHg levels on the mitochondrial oxidative status and to evaluate the niacin protective effect against MeHg-induced oxidative stress. For this purpose, Male Wistar rats were divided into four groups: control group, treated with drinking water on a daily basis; group exposed to MeHg at a dose of 100 µg/kg/day; group that received niacin at a dose of 50 mg/kg/day in drinking water, with drinking water being administered by gavage; group that received niacin at a dose of 50 mg/kg/day in drinking water as well as MeHg at a dose of 100 µg/kg/day. After 12 weeks, the rats, which weighed 500–550 g, were sacrificed, and their liver mitochondria were isolated by standard differential centrifugation. Sub-chronic exposure to MeHg (100 µg/kg/day for 12 weeks) led to mitochondrial swelling (p < 0.05) and induced ROS overproduction as determined by increased DFCH oxidation (p < 0.05), increased gluthatione oxidation (p < 0.05), and reduced protein thiol content (p < 0.05). In contrast, niacin supplementation inhibited oxidative stress, which counteracted and minimized the toxic MeHg effects on mitochondria. |
publishDate |
2018 |
dc.date.none.fl_str_mv |
2018-12-11T17:22:43Z 2018-12-11T17:22:43Z 2018-01-01 |
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/10.1080/01480545.2018.1497045 Drug and Chemical Toxicology. 1525-6014 0148-0545 http://hdl.handle.net/11449/176841 10.1080/01480545.2018.1497045 2-s2.0-85053294086 186557912427276 |
url |
http://dx.doi.org/10.1080/01480545.2018.1497045 http://hdl.handle.net/11449/176841 |
identifier_str_mv |
Drug and Chemical Toxicology. 1525-6014 0148-0545 10.1080/01480545.2018.1497045 2-s2.0-85053294086 186557912427276 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Drug and Chemical Toxicology 0,460 0,460 |
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 |
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UNESP |
reponame_str |
Repositório Institucional da UNESP |
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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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