p53- and Caspase-3-Independent Mechanism of Acetaminophen Effect on Human Neural Cells
Acetaminophen in a concentration of 5 mM increased the expression of JNK , HIF1A (hypoxiainduced factor), and CASP3 , which indicated development of oxidative stress and apoptotic cell death. Acetaminophen in a concentration of 10 mM did not induce expression of HIF1A and CASP3 , but reduced express...
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Veröffentlicht in: | Bulletin of experimental biology and medicine 2016-04, Vol.160 (6), p.763-766 |
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container_title | Bulletin of experimental biology and medicine |
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creator | Aleksandrova, A. V. Senyavina, N. V. Maltseva, D. V. Khutornenko, A. A. Sakharov, D. A. |
description | Acetaminophen in a concentration of 5 mM increased the expression of
JNK
,
HIF1A
(hypoxiainduced factor), and
CASP3
, which indicated development of oxidative stress and apoptotic cell death. Acetaminophen in a concentration of 10 mM did not induce expression of
HIF1A
and
CASP3
, but reduced expression of chaperone
HSP90
, which attested to activation of a caspase-3-independent mechanism of cell death. The methods of preventing acetaminophen intoxication are discussed. |
doi_str_mv | 10.1007/s10517-016-3304-7 |
format | Article |
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JNK
,
HIF1A
(hypoxiainduced factor), and
CASP3
, which indicated development of oxidative stress and apoptotic cell death. Acetaminophen in a concentration of 10 mM did not induce expression of
HIF1A
and
CASP3
, but reduced expression of chaperone
HSP90
, which attested to activation of a caspase-3-independent mechanism of cell death. The methods of preventing acetaminophen intoxication are discussed.</description><identifier>ISSN: 0007-4888</identifier><identifier>EISSN: 1573-8221</identifier><identifier>DOI: 10.1007/s10517-016-3304-7</identifier><identifier>PMID: 27165078</identifier><identifier>CODEN: BEXBAN</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Acetaminophen ; Acetaminophen - pharmacology ; Analgesics, Non-Narcotic - pharmacology ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Caspase 3 - metabolism ; Cell Biology ; Cell death ; Cell Line, Tumor ; Cell Survival - drug effects ; Gene Expression - drug effects ; Heat shock proteins ; Humans ; Internal Medicine ; Laboratory Medicine ; Neurons - drug effects ; Oxidative Stress ; Pathology ; Physiological aspects ; Tumor proteins ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Bulletin of experimental biology and medicine, 2016-04, Vol.160 (6), p.763-766</ispartof><rights>Springer Science+Business Media New York 2016</rights><rights>COPYRIGHT 2016 Springer</rights><rights>Bulletin of Experimental Biology and Medicine is a copyright of Springer, 2016.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-4d61a31464a185afdd985b3aaa7dfb8f998d773f280c9b9799eaf71a625232ec3</citedby><cites>FETCH-LOGICAL-c503t-4d61a31464a185afdd985b3aaa7dfb8f998d773f280c9b9799eaf71a625232ec3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10517-016-3304-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10517-016-3304-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41466,42535,51296</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27165078$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aleksandrova, A. V.</creatorcontrib><creatorcontrib>Senyavina, N. V.</creatorcontrib><creatorcontrib>Maltseva, D. V.</creatorcontrib><creatorcontrib>Khutornenko, A. A.</creatorcontrib><creatorcontrib>Sakharov, D. A.</creatorcontrib><title>p53- and Caspase-3-Independent Mechanism of Acetaminophen Effect on Human Neural Cells</title><title>Bulletin of experimental biology and medicine</title><addtitle>Bull Exp Biol Med</addtitle><addtitle>Bull Exp Biol Med</addtitle><description>Acetaminophen in a concentration of 5 mM increased the expression of
JNK
,
HIF1A
(hypoxiainduced factor), and
CASP3
, which indicated development of oxidative stress and apoptotic cell death. Acetaminophen in a concentration of 10 mM did not induce expression of
HIF1A
and
CASP3
, but reduced expression of chaperone
HSP90
, which attested to activation of a caspase-3-independent mechanism of cell death. The methods of preventing acetaminophen intoxication are discussed.</description><subject>Acetaminophen</subject><subject>Acetaminophen - pharmacology</subject><subject>Analgesics, Non-Narcotic - pharmacology</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Biology</subject><subject>Cell death</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>Gene Expression - drug effects</subject><subject>Heat shock proteins</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Laboratory Medicine</subject><subject>Neurons - drug effects</subject><subject>Oxidative Stress</subject><subject>Pathology</subject><subject>Physiological aspects</subject><subject>Tumor proteins</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>0007-4888</issn><issn>1573-8221</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkl1rFDEYhYModq3-AG8kIIg3qfmYTDKXy1JtoR836m14N_OmO2UmGSczF_33ZtmqrVgkkPAmzznkwCHkreAngnPzKQuuhWFc1EwpXjHzjKyENopZKcVzsuIFYpW19oi8yvl2P_JavCRH0ohac2NX5PuoFaMQW7qBPEJGpth5bHHEssWZXqLfQezyQFOga48zDF1M4w4jPQ0B_UxTpGfLAJFe4TJBTzfY9_k1eRGgz_jm_jwm3z6fft2csYvrL-eb9QXzmquZVW0tQImqrkBYDaFtG6u3CgBMG7Y2NI1tjVFBWu6bbWOaBiEYAbXUUkn06ph8PPiOU_qxYJ7d0GVffgAR05KdsEI0XEpT_x81Da9qYwQv6Pu_0Nu0TLEEKYY1t400lfxD3UCProshzRP4valbV1pLa7iqCnXyD6qsFofOp4ihK_ePBB8eCHYI_bzLqV_mLsX8GBQH0E8p5wmDG6dugOnOCe72_XCHfrjSD7fvhzNF8-4-2bIdsP2t-FWIAsgDkMtTvMHpQfQnXX8CIkO_7A</recordid><startdate>20160401</startdate><enddate>20160401</enddate><creator>Aleksandrova, A. V.</creator><creator>Senyavina, N. V.</creator><creator>Maltseva, D. V.</creator><creator>Khutornenko, A. A.</creator><creator>Sakharov, D. 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V. ; Senyavina, N. V. ; Maltseva, D. V. ; Khutornenko, A. A. ; Sakharov, D. A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-4d61a31464a185afdd985b3aaa7dfb8f998d773f280c9b9799eaf71a625232ec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Acetaminophen</topic><topic>Acetaminophen - pharmacology</topic><topic>Analgesics, Non-Narcotic - pharmacology</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Biology</topic><topic>Cell death</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival - drug effects</topic><topic>Gene Expression - drug effects</topic><topic>Heat shock proteins</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Laboratory Medicine</topic><topic>Neurons - drug effects</topic><topic>Oxidative Stress</topic><topic>Pathology</topic><topic>Physiological aspects</topic><topic>Tumor proteins</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aleksandrova, A. 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JNK
,
HIF1A
(hypoxiainduced factor), and
CASP3
, which indicated development of oxidative stress and apoptotic cell death. Acetaminophen in a concentration of 10 mM did not induce expression of
HIF1A
and
CASP3
, but reduced expression of chaperone
HSP90
, which attested to activation of a caspase-3-independent mechanism of cell death. The methods of preventing acetaminophen intoxication are discussed.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>27165078</pmid><doi>10.1007/s10517-016-3304-7</doi><tpages>4</tpages></addata></record> |
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subjects | Acetaminophen Acetaminophen - pharmacology Analgesics, Non-Narcotic - pharmacology Apoptosis Biomedical and Life Sciences Biomedicine Caspase 3 - metabolism Cell Biology Cell death Cell Line, Tumor Cell Survival - drug effects Gene Expression - drug effects Heat shock proteins Humans Internal Medicine Laboratory Medicine Neurons - drug effects Oxidative Stress Pathology Physiological aspects Tumor proteins Tumor Suppressor Protein p53 - metabolism |
title | p53- and Caspase-3-Independent Mechanism of Acetaminophen Effect on Human Neural Cells |
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