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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1995-8-3
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pubmed:abstractText |
Acetaminophen (APAP) intoxication has been shown to activate Kupffer cells. Kupffer cell activation is also associated with the release of proinflammatory cytokines which can induce a variety of pathophysiological responses. These studies examined whether proinflammatory cytokines are produced in response to a hepatotoxic dose of APAP, and if so, the role they play in the observed pathological response. Female B6C3F1 mice received 500 mg APAP/kg in the presence and absence of antibodies against tumor necrosis factor-alpha (TNF-alpha), interleukin-1-alpha (IL-1 alpha), and IL-1 receptor antagonist (IL-1ra). Serum TNF-alpha, IL-1 alpha, and liver-associated enzyme levels were measured. In addition, the levels of mRNA transcripts for IL-1 alpha, IL-6, and TNF-alpha from livers of treated mice were examined by reverse transcription-polymerase chain reaction (RT-PCR). Administration of APAP resulted in an immediate reduction in body temperature as well as elevated serum levels of IL-1 alpha and TNF-alpha that reached a peak at 12 and 16 hr, respectively. The reduction in body temperature was partially blocked by injection of antibodies against TNF-alpha or IL-1 alpha. Furthermore, neutralization of TNF-alpha delayed the increase in serum IL-1 alpha and liver enzyme levels. In contrast, pretreatment with IL-1ra antisera exacerbated the effect of APAP on body temperature and increased the release of liver enzymes. These data suggest that TNF-alpha and IL-1 alpha are released in response to APAP intoxication and are responsible for certain pathological manifestations of APAP-induced hepatotoxicity.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acetaminophen,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Il1rn protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin 1 Receptor Antagonist...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Sialoglycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0041-008X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
133
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
43-52
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7597709-Acetaminophen,
pubmed-meshheading:7597709-Animals,
pubmed-meshheading:7597709-Base Sequence,
pubmed-meshheading:7597709-Cytokines,
pubmed-meshheading:7597709-Female,
pubmed-meshheading:7597709-Gene Expression,
pubmed-meshheading:7597709-Interleukin 1 Receptor Antagonist Protein,
pubmed-meshheading:7597709-Interleukin-1,
pubmed-meshheading:7597709-Liver,
pubmed-meshheading:7597709-Mice,
pubmed-meshheading:7597709-Mice, Inbred C3H,
pubmed-meshheading:7597709-Mice, Inbred C57BL,
pubmed-meshheading:7597709-Molecular Sequence Data,
pubmed-meshheading:7597709-Sialoglycoproteins,
pubmed-meshheading:7597709-Tumor Necrosis Factor-alpha
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pubmed:year |
1995
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pubmed:articleTitle |
Role of proinflammatory cytokines in acetaminophen hepatotoxicity.
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pubmed:affiliation |
Environmental Immunology and Neurobiology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.
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pubmed:publicationType |
Journal Article
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