pubmed-article:12100152 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12100152 | lifeskim:mentions | umls-concept:C0003402 | lld:lifeskim |
pubmed-article:12100152 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:12100152 | lifeskim:mentions | umls-concept:C0027540 | lld:lifeskim |
pubmed-article:12100152 | lifeskim:mentions | umls-concept:C0376448 | lld:lifeskim |
pubmed-article:12100152 | lifeskim:mentions | umls-concept:C0000894 | lld:lifeskim |
pubmed-article:12100152 | lifeskim:mentions | umls-concept:C0439836 | lld:lifeskim |
pubmed-article:12100152 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:12100152 | pubmed:dateCreated | 2002-7-8 | lld:pubmed |
pubmed-article:12100152 | pubmed:abstractText | We treated rapidly growing Jurkat cells with 40 nmol/l of doxorubicin for 72 h. After 36 h, the G2-arrested cells became larger and some of them started endoreplication. Nuclear staining with Hoechst 33342 combined with propidium iodide (PI) exclusion revealed that about 90% of the cells were necrotic at 72 h, although apoptotic cells accounted for only 8%. Incubation with 40 nmol/l of aclarubicin or cytosine beta-d-arabinofuranoside for 60 h induced necrosis both in Jurkat and ml-1 cells. Pre-necrotic Jurkat cells incubated with 40 nmol/l of doxorubicin had much higher intracellular reactive oxygen species (ROS) levels than pre-apoptotic ones. Addition of Tempol or Desferal accelerated doxorubicin-induced necrosis and partially converted it into apoptosis. Both antioxidants reduced surviving colony numbers of prenecrotic Jurkat cells. n-acetyl-l-cysteine had little effect on the apoptotic conversion but profoundly accelerated necrosis. Because an apoptosis-resistant Jurkat subclone was also refractory to doxorubicin-induced necrosis, apoptosis and necrosis might share some common pathways. Low-dose doxorubicin increased micronuclei-positive cell percentages and also suppressed high-dose doxorubicin-induced apoptosis in Jurkat and ml-1 cells. Some of the prenecrotic cells, therefore, might survive and obtain genomic instability. Antioxidants may be useful to suppress, at least to some extent, this vicious consequence. | lld:pubmed |
pubmed-article:12100152 | pubmed:language | eng | lld:pubmed |
pubmed-article:12100152 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12100152 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12100152 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12100152 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12100152 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12100152 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12100152 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12100152 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12100152 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12100152 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12100152 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12100152 | pubmed:month | Jul | lld:pubmed |
pubmed-article:12100152 | pubmed:issn | 0007-1048 | lld:pubmed |
pubmed-article:12100152 | pubmed:author | pubmed-author:SasakiMakotoM | lld:pubmed |
pubmed-article:12100152 | pubmed:author | pubmed-author:SugimotoKoich... | lld:pubmed |
pubmed-article:12100152 | pubmed:author | pubmed-author:OshimiKazuoK | lld:pubmed |
pubmed-article:12100152 | pubmed:author | pubmed-author:TamayoseKenji... | lld:pubmed |
pubmed-article:12100152 | pubmed:author | pubmed-author:HayashiKeikoK | lld:pubmed |
pubmed-article:12100152 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12100152 | pubmed:volume | 118 | lld:pubmed |
pubmed-article:12100152 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12100152 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12100152 | pubmed:pagination | 229-38 | lld:pubmed |
pubmed-article:12100152 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:12100152 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:12100152 | pubmed:articleTitle | Low-dose doxorubicin-induced necrosis in Jurkat cells and its acceleration and conversion to apoptosis by antioxidants. | lld:pubmed |
pubmed-article:12100152 | pubmed:affiliation | Department of Haematology, Juntendo University School of Medicine, Tokyo, Japan. ksugimot@med.juntendo.ac.jp | lld:pubmed |
pubmed-article:12100152 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12100152 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:12100152 | lld:pubmed |