The bipyridyl herbicide paraquat produces oxidative stress-mediated toxicity in human neuroblastoma SH-SY5Y cells: relevance to the dopaminergic pathogenesis.
Identifieur interne : 001223 ( PubMed/Corpus ); précédent : 001222; suivant : 001224The bipyridyl herbicide paraquat produces oxidative stress-mediated toxicity in human neuroblastoma SH-SY5Y cells: relevance to the dopaminergic pathogenesis.
Auteurs : Wonsuk Yang ; Evelyn Tiffany-CastiglioniSource :
- Journal of toxicology and environmental health. Part A [ 1528-7394 ] ; 2005.
English descriptors
- KwdEn :
- Dopamine Plasma Membrane Transport Proteins, Glutathione (metabolism), Glutathione Transferase (metabolism), Herbicides (pharmacology), Herbicides (toxicity), Humans, Membrane Glycoproteins (drug effects), Membrane Glycoproteins (physiology), Membrane Transport Proteins (drug effects), Membrane Transport Proteins (physiology), Nerve Tissue Proteins (drug effects), Nerve Tissue Proteins (physiology), Neuroblastoma (pathology), Neurons, Oxidative Stress, Paraquat (pharmacology), Paraquat (toxicity), Parkinson Disease (physiopathology), Reactive Oxygen Species, Receptors, Dopamine (drug effects), Receptors, Dopamine (physiology), Tumor Cells, Cultured (pathology).
- MESH :
- chemical , drug effects : Membrane Glycoproteins, Membrane Transport Proteins, Nerve Tissue Proteins, Receptors, Dopamine.
- chemical , metabolism : Glutathione, Glutathione Transferase.
- chemical , pharmacology : Herbicides, Paraquat.
- chemical , physiology : Membrane Glycoproteins, Membrane Transport Proteins, Nerve Tissue Proteins, Receptors, Dopamine.
- chemical , toxicity : Herbicides, Paraquat.
- chemical : Dopamine Plasma Membrane Transport Proteins, Reactive Oxygen Species.
- pathology : Neuroblastoma, Tumor Cells, Cultured.
- physiopathology : Parkinson Disease.
- Humans, Neurons, Oxidative Stress.
Abstract
Paraquat (PQ) is a cationic nonselective bipyridyl herbicide widely used to control weeds and grasses in agriculture. Epidemiologic studies indicate that exposure to pesticides can be a risk factor in the incidence of Parkinson's disease (PD). A strong correlation has been reported between exposure to paraquat and PD incidence in Canada, Taiwan, and the United States. This correlation is supported by animal studies showing that paraquat produces toxicity in dopaminergic neurons of the rat and mouse brain. However, it is unclear how paraquat triggers toxicity in dopaminergic neurons. Based on the prooxidant properties of paraquat, it was hypothesized that paraquat may induce oxidative stress-mediated toxicity in dopaminergic neurons. To explore this possibility, dopaminergic SH-SY5Y cells were treated with paraquat, and several biomarkers of oxidativestress were measured. First, a specific dopamine transporter inhibitor GBR12909 significantly protected SY5Y cells against the toxicity of paraquat, indicating that paraquat exerts its toxicity by a mechanism involving the dopamine transporter (DAT). Second, paraquat increased intracellular levels of reactive oxygen species (ROS), but decreased the levels of glutathione. Third, paraquat inhibited glutathione peroxidase activity, but did not affect glutathione reductase activity. On the other hand, paraquat increased GST activity by 24 h, after which GST activity returned to the control value at 48 h. Fourth, paraquat dissipated mitochondrial transmembrane potential (MTP). Fifth, paraquat produced increases of malondialdehyde (MDA) and protein carbonyls, as well as DNA fragmentation, indicating oxidative damage to major cellular components. Sixth, paraquat increased the protein level of heme oxygenase-1 (HO-1). Taken together, these findings verify our hypothesis that paraquat produces oxidative stress-mediated toxicity in SH-SY5Y cells. Thus, current findings suggest that paraquat may induce the pathogenesis of dopaminergic neurons through oxidative stress.
DOI: 10.1080/15287390500226987
PubMed: 16263688
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pubmed:16263688Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The bipyridyl herbicide paraquat produces oxidative stress-mediated toxicity in human neuroblastoma SH-SY5Y cells: relevance to the dopaminergic pathogenesis.</title><author><name sortKey="Yang, Wonsuk" sort="Yang, Wonsuk" uniqKey="Yang W" first="Wonsuk" last="Yang">Wonsuk Yang</name><affiliation><nlm:affiliation>Department of Integrative Biosciences, Texas A&M University, College Station, Texas 77843, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Tiffany Castiglioni, Evelyn" sort="Tiffany Castiglioni, Evelyn" uniqKey="Tiffany Castiglioni E" first="Evelyn" last="Tiffany-Castiglioni">Evelyn Tiffany-Castiglioni</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:16263688</idno><idno type="pmid">16263688</idno><idno type="doi">10.1080/15287390500226987</idno><idno type="wicri:Area/PubMed/Corpus">001223</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001223</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The bipyridyl herbicide paraquat produces oxidative stress-mediated toxicity in human neuroblastoma SH-SY5Y cells: relevance to the dopaminergic pathogenesis.</title><author><name sortKey="Yang, Wonsuk" sort="Yang, Wonsuk" uniqKey="Yang W" first="Wonsuk" last="Yang">Wonsuk Yang</name><affiliation><nlm:affiliation>Department of Integrative Biosciences, Texas A&M University, College Station, Texas 77843, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Tiffany Castiglioni, Evelyn" sort="Tiffany Castiglioni, Evelyn" uniqKey="Tiffany Castiglioni E" first="Evelyn" last="Tiffany-Castiglioni">Evelyn Tiffany-Castiglioni</name></author></analytic><series><title level="j">Journal of toxicology and environmental health. Part A</title><idno type="ISSN">1528-7394</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dopamine Plasma Membrane Transport Proteins</term><term>Glutathione (metabolism)</term><term>Glutathione Transferase (metabolism)</term><term>Herbicides (pharmacology)</term><term>Herbicides (toxicity)</term><term>Humans</term><term>Membrane Glycoproteins (drug effects)</term><term>Membrane Glycoproteins (physiology)</term><term>Membrane Transport Proteins (drug effects)</term><term>Membrane Transport Proteins (physiology)</term><term>Nerve Tissue Proteins (drug effects)</term><term>Nerve Tissue Proteins (physiology)</term><term>Neuroblastoma (pathology)</term><term>Neurons</term><term>Oxidative Stress</term><term>Paraquat (pharmacology)</term><term>Paraquat (toxicity)</term><term>Parkinson Disease (physiopathology)</term><term>Reactive Oxygen Species</term><term>Receptors, Dopamine (drug effects)</term><term>Receptors, Dopamine (physiology)</term><term>Tumor Cells, Cultured (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Nerve Tissue Proteins</term><term>Receptors, Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutathione</term><term>Glutathione Transferase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Herbicides</term><term>Paraquat</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Nerve Tissue Proteins</term><term>Receptors, Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Herbicides</term><term>Paraquat</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Dopamine Plasma Membrane Transport Proteins</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neuroblastoma</term><term>Tumor Cells, Cultured</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Neurons</term><term>Oxidative Stress</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Paraquat (PQ) is a cationic nonselective bipyridyl herbicide widely used to control weeds and grasses in agriculture. Epidemiologic studies indicate that exposure to pesticides can be a risk factor in the incidence of Parkinson's disease (PD). A strong correlation has been reported between exposure to paraquat and PD incidence in Canada, Taiwan, and the United States. This correlation is supported by animal studies showing that paraquat produces toxicity in dopaminergic neurons of the rat and mouse brain. However, it is unclear how paraquat triggers toxicity in dopaminergic neurons. Based on the prooxidant properties of paraquat, it was hypothesized that paraquat may induce oxidative stress-mediated toxicity in dopaminergic neurons. To explore this possibility, dopaminergic SH-SY5Y cells were treated with paraquat, and several biomarkers of oxidativestress were measured. First, a specific dopamine transporter inhibitor GBR12909 significantly protected SY5Y cells against the toxicity of paraquat, indicating that paraquat exerts its toxicity by a mechanism involving the dopamine transporter (DAT). Second, paraquat increased intracellular levels of reactive oxygen species (ROS), but decreased the levels of glutathione. Third, paraquat inhibited glutathione peroxidase activity, but did not affect glutathione reductase activity. On the other hand, paraquat increased GST activity by 24 h, after which GST activity returned to the control value at 48 h. Fourth, paraquat dissipated mitochondrial transmembrane potential (MTP). Fifth, paraquat produced increases of malondialdehyde (MDA) and protein carbonyls, as well as DNA fragmentation, indicating oxidative damage to major cellular components. Sixth, paraquat increased the protein level of heme oxygenase-1 (HO-1). Taken together, these findings verify our hypothesis that paraquat produces oxidative stress-mediated toxicity in SH-SY5Y cells. Thus, current findings suggest that paraquat may induce the pathogenesis of dopaminergic neurons through oxidative stress.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16263688</PMID><DateCreated><Year>2005</Year><Month>11</Month><Day>02</Day></DateCreated><DateCompleted><Year>2005</Year><Month>11</Month><Day>15</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1528-7394</ISSN><JournalIssue CitedMedium="Print"><Volume>68</Volume><Issue>22</Issue><PubDate><Year>2005</Year><Month>Nov</Month><Day>26</Day></PubDate></JournalIssue><Title>Journal of toxicology and environmental health. Part A</Title><ISOAbbreviation>J. Toxicol. Environ. Health Part A</ISOAbbreviation></Journal><ArticleTitle>The bipyridyl herbicide paraquat produces oxidative stress-mediated toxicity in human neuroblastoma SH-SY5Y cells: relevance to the dopaminergic pathogenesis.</ArticleTitle><Pagination><MedlinePgn>1939-61</MedlinePgn></Pagination><Abstract><AbstractText>Paraquat (PQ) is a cationic nonselective bipyridyl herbicide widely used to control weeds and grasses in agriculture. Epidemiologic studies indicate that exposure to pesticides can be a risk factor in the incidence of Parkinson's disease (PD). A strong correlation has been reported between exposure to paraquat and PD incidence in Canada, Taiwan, and the United States. This correlation is supported by animal studies showing that paraquat produces toxicity in dopaminergic neurons of the rat and mouse brain. However, it is unclear how paraquat triggers toxicity in dopaminergic neurons. Based on the prooxidant properties of paraquat, it was hypothesized that paraquat may induce oxidative stress-mediated toxicity in dopaminergic neurons. To explore this possibility, dopaminergic SH-SY5Y cells were treated with paraquat, and several biomarkers of oxidativestress were measured. First, a specific dopamine transporter inhibitor GBR12909 significantly protected SY5Y cells against the toxicity of paraquat, indicating that paraquat exerts its toxicity by a mechanism involving the dopamine transporter (DAT). Second, paraquat increased intracellular levels of reactive oxygen species (ROS), but decreased the levels of glutathione. Third, paraquat inhibited glutathione peroxidase activity, but did not affect glutathione reductase activity. On the other hand, paraquat increased GST activity by 24 h, after which GST activity returned to the control value at 48 h. Fourth, paraquat dissipated mitochondrial transmembrane potential (MTP). Fifth, paraquat produced increases of malondialdehyde (MDA) and protein carbonyls, as well as DNA fragmentation, indicating oxidative damage to major cellular components. Sixth, paraquat increased the protein level of heme oxygenase-1 (HO-1). Taken together, these findings verify our hypothesis that paraquat produces oxidative stress-mediated toxicity in SH-SY5Y cells. 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