Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/33173
DC FieldValueLanguage
dc.contributor.authorLiao, J.W.en_US
dc.contributor.author廖俊旺zh_TW
dc.contributor.authorKang, J.J.en_US
dc.contributor.authorJeng, C.R.en_US
dc.contributor.authorChang, S.K.en_US
dc.contributor.authorKuo, M.J.en_US
dc.contributor.authorWang, S.C.en_US
dc.contributor.authorLiu, M.R.S.en_US
dc.contributor.authorPang, V.F.en_US
dc.date2006zh_TW
dc.date.accessioned2014-06-06T07:45:04Z-
dc.date.available2014-06-06T07:45:04Z-
dc.identifier.issn0300-483Xzh_TW
dc.identifier.urihttp://hdl.handle.net/11455/33173-
dc.description.abstractOur previous study has demonstrated that instead of neuromuscular blockage cartap, an orgationitrogen insecticide, could cause a marked irreversible Ca2+-dependent contracture in both isolated mouse and rabbit phrenic nerve-diaphragms. We further examined the potential of direct myocytotoxicity of cartap and the possible roles of calcium ion and oxidative stress on cartap-induced muscle cell injury using the mouse myoblast cell line, C2C12. Cartap exerted a dose- and time-dependent cytotoxic effect in C2C12 cells measured by MTT colorimetric assay and trypan blue dye exclusion. The extracellular activities of both creatine kinase (CK) and lactate dehydrogenase (LDH) were elevated in the cartap-treated groups at or greater than 100 mu M. The isoenzymatic profiles showed that the elevations were mainly due to CK-3, LDH-3, and LDH-4, Following the addition of 0.5-2.5 mM EGTA, a Ca2+ chelator, or 30-100 mu M verapamil, an L-type Ca2+ channel blocker, the cartap-induced reduction in MTT metabolic rate of C2C12 cells was significantly restored in a dose-dependent manner in both EGTA and verapamil-treated cells. Furthermore, EGTA could significantly reduce the cartap-induced elevation in the levels of total extracellular CK and LDH activities. Additionally, cartap significantly increased the level of endogenous reactive oxygen species (ROS) in C2C12 cells in a dose- and time-dependent manner. The cartap-induced ROS generation could be significantly inhibited by antioxidants, including Vitamins C and E, catalase, and superoxide dismutase, with catalase the most effective. EGTA could significantly inhibit cartap-induced ROS generation in a dose-dependent manner. The results suggested that cartap could induce ROS generation in C2C12 cells via a Ca2+-dependant mechanism resulting in subsequent cytotoxicity, at least partially, to C2C12 cells. It is speculated that both Ca2+ and Ca2+-induced ROS may also play the central role on the myogenic contracture and myofiber injury of the diaphragm leading to respiratory failure and subsequent death in rabbits exposed ocularly to cartap. (c) 2005 Elsevier Ireland Ltd. All rights reserved.en_US
dc.language.isoen_USzh_TW
dc.relationToxicologyen_US
dc.relation.ispartofseriesToxicology, Volume 219, Issue 1-3, Page(s) 73-84.en_US
dc.relation.urihttp://dx.doi.org/10.1016/j.tox.2005.11.002en_US
dc.subjectcartapen_US
dc.subjectcytotoxicityen_US
dc.subjectoxidative stressen_US
dc.subjectCa2+en_US
dc.subjectC2C12 cellsen_US
dc.subjectin vitroen_US
dc.subjectmodelen_US
dc.subjectskeletal-muscleen_US
dc.subjectdiaphragm muscleen_US
dc.subjectgenerationen_US
dc.subjectinjuryen_US
dc.subjectmitochondrialen_US
dc.subjectexpressionen_US
dc.subjectmemantineen_US
dc.subjectviabilityen_US
dc.subjectperoxideen_US
dc.subjectexposureen_US
dc.titleCartap-induced cytotoxicity in mouse C2C12 myoblast cell line and the roles of calcium ion and oxidative stress on the toxic effectsen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1016/j.tox.2005.11.002zh_TW
item.fulltextno fulltext-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.languageiso639-1en_US-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
Appears in Collections:獸醫病理生物學所
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