| pubmed-article:10079182 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10079182 | lifeskim:mentions | umls-concept:C0007765 | lld:lifeskim |
| pubmed-article:10079182 | lifeskim:mentions | umls-concept:C0596630 | lld:lifeskim |
| pubmed-article:10079182 | lifeskim:mentions | umls-concept:C0162772 | lld:lifeskim |
| pubmed-article:10079182 | lifeskim:mentions | umls-concept:C0449416 | lld:lifeskim |
| pubmed-article:10079182 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
| pubmed-article:10079182 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:10079182 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:10079182 | pubmed:dateCreated | 1999-4-13 | lld:pubmed |
| pubmed-article:10079182 | pubmed:abstractText | Reactive oxygen species (ROS) production in rat cerebellar granule cells in the presence of the excitotoxins N-methyl-d-aspartate (NMDA) and kainic acid (KA) and by the protein kinase C activator phorbol myristate acetate (PMA) was Ca2+-dependent and resulted in decreased cell viability. Exposure of stimulated cells to rotenone (a respiratory chain inhibitor) did not decrease ROS levels and did not affect short-term cell viability. In cells stimulated by NMDA and KA, exposure to indomethacin (a cyclooxygenase inhibitor) and nialamide (a monoamine oxidase inhibitor) caused a decrease in ROS levels and increased cell viability occurred in NMDA-treated cells. In contrast, PMA-stimulated neurons did not show decreased ROS levels when exposed to indomethacin and nialamide. These studies suggest that there is a multiplicity of routes for Ca2+-dependent ROS production in neurons but that ROS generation by cyclooxygenase and monoamine oxidase is not controlled by protein kinase C. | lld:pubmed |
| pubmed-article:10079182 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10079182 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10079182 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10079182 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10079182 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10079182 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10079182 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10079182 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10079182 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10079182 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10079182 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10079182 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10079182 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:10079182 | pubmed:issn | 0006-291X | lld:pubmed |
| pubmed-article:10079182 | pubmed:author | pubmed-author:CarpenterD... | lld:pubmed |
| pubmed-article:10079182 | pubmed:author | pubmed-author:BoldyrevA AAA | lld:pubmed |
| pubmed-article:10079182 | pubmed:author | pubmed-author:JohnsonPP | lld:pubmed |
| pubmed-article:10079182 | pubmed:author | pubmed-author:PetersC MCM | lld:pubmed |
| pubmed-article:10079182 | pubmed:author | pubmed-author:HuentelmanM... | lld:pubmed |
| pubmed-article:10079182 | pubmed:copyrightInfo | Copyright 1999 Academic Press. | lld:pubmed |
| pubmed-article:10079182 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10079182 | pubmed:day | 16 | lld:pubmed |
| pubmed-article:10079182 | pubmed:volume | 256 | lld:pubmed |
| pubmed-article:10079182 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10079182 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10079182 | pubmed:pagination | 320-4 | lld:pubmed |
| pubmed-article:10079182 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:10079182 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10079182 | pubmed:articleTitle | Sources of reactive oxygen species production in excitotoxin- stimulated cerebellar granule cells. | lld:pubmed |
| pubmed-article:10079182 | pubmed:affiliation | Department of Biochemistry, International Biotechnological Center of M. V. Lomonosov Moscow State University, Moscow, 119899, Russia. | lld:pubmed |
| pubmed-article:10079182 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10079182 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10079182 | lld:pubmed |
