Glutathione peroxidase-1 overexpressing transgenic mice are protected from neurotoxicity induced by microcystin-leucine-arginine
DC Field | Value | Language |
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dc.contributor.author | Shin, Eun-Joo | - |
dc.contributor.author | Hwang, Yeong Gwang | - |
dc.contributor.author | Duc Toan Pham | - |
dc.contributor.author | Lee, Ji Won | - |
dc.contributor.author | Lee, Yu Jeung | - |
dc.contributor.author | Pyo, Dongjin | - |
dc.contributor.author | Jeong, Ji Hoon | - |
dc.contributor.author | Lei, Xin Gen | - |
dc.contributor.author | Kim, Hyoung-Chun | - |
dc.date.available | 2019-01-22T12:34:44Z | - |
dc.date.issued | 2018-10 | - |
dc.identifier.issn | 1520-4081 | - |
dc.identifier.issn | 1522-7278 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/694 | - |
dc.description.abstract | Although it has been well-recognized that microcystin-leucine-arginine (MCLR), the most common form of microcystins, induces neurotoxicity, little is currently known about the underlying mechanism for this neurotoxicity. Here, we found that MCLR (10 ng/L/mouse, i.c.v.) induces significant neuronal loss in the hippocampus of mice. MCLR-induced neurotoxicity was accompanied by oxidative stress, as shown by a significant increase in the level of 4-hydroxynonenal, protein carbonyl, and reactive oxygen species (ROS). Superoxide dismutase-1 (SOD-1) activity was significantly increased, but glutathione peroxidase (GPx) level was significantly decreased following MCLR insult. In addition, MCLR significantly inhibited GSH/GSSG ratio, and significantly induced NFB DNA binding activity. Because reduced activity of GPx appeared to be critical for the imbalance between activities of SODs and GPx, we utilized GPx-1 overexpressing transgenic mice to ascertain the role of GPx-1 in this neurotoxicity. Genetic overexpression of GPx-1 or NFB inhibitor pyrrolidine dithiocarbamate (PDTC) significantly attenuated MCLR-induced hippocampal neuronal loss in mice. However, PDTC did not exert any additive effect on neuroprotection mediated by GPx-1 overexpression, indicating that NFB is a neurotoxic target of MCLR. Combined, these results suggest that MCLR-induced neurotoxicity requires oxidative stress associated with failure in compensatory induction of GPx, possibly through activation of the transcription factor NFB. | - |
dc.format.extent | 10 | - |
dc.publisher | WILEY | - |
dc.title | Glutathione peroxidase-1 overexpressing transgenic mice are protected from neurotoxicity induced by microcystin-leucine-arginine | - |
dc.type | Article | - |
dc.identifier.doi | 10.1002/tox.22580 | - |
dc.identifier.bibliographicCitation | ENVIRONMENTAL TOXICOLOGY, v.33, no.10, pp 1019 - 1028 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000444226600002 | - |
dc.identifier.scopusid | 2-s2.0-85052658772 | - |
dc.citation.endPage | 1028 | - |
dc.citation.number | 10 | - |
dc.citation.startPage | 1019 | - |
dc.citation.title | ENVIRONMENTAL TOXICOLOGY | - |
dc.citation.volume | 33 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordAuthor | GPx-1 overexpressing transgenic mice | - |
dc.subject.keywordAuthor | hippocampus | - |
dc.subject.keywordAuthor | intracerebroventricular infusion | - |
dc.subject.keywordAuthor | microcystin-leucine-arginine | - |
dc.subject.keywordAuthor | neurotoxicity | - |
dc.subject.keywordAuthor | NFB | - |
dc.subject.keywordPlus | INDUCED OXIDATIVE STRESS | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | SUPERCRITICAL-FLUID EXTRACTION | - |
dc.subject.keywordPlus | LR-INDUCED HEPATOTOXICITY | - |
dc.subject.keywordPlus | CYCLIC PEPTIDE TOXIN | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | CYANOBACTERIAL TOXINS | - |
dc.subject.keywordPlus | ANTIOXIDANT ENZYMES | - |
dc.subject.keywordPlus | PROTEOMIC ANALYSIS | - |
dc.subject.keywordPlus | DRINKING-WATER | - |
dc.relation.journalResearchArea | Environmental Sciences & Ecology | - |
dc.relation.journalResearchArea | Toxicology | - |
dc.relation.journalResearchArea | Water Resources | - |
dc.relation.journalWebOfScienceCategory | Environmental Sciences | - |
dc.relation.journalWebOfScienceCategory | Toxicology | - |
dc.relation.journalWebOfScienceCategory | Water Resources | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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