pubmed-article:8786558 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8786558 | lifeskim:mentions | umls-concept:C0009170 | lld:lifeskim |
pubmed-article:8786558 | lifeskim:mentions | umls-concept:C0025519 | lld:lifeskim |
pubmed-article:8786558 | lifeskim:mentions | umls-concept:C0021080 | lld:lifeskim |
pubmed-article:8786558 | lifeskim:mentions | umls-concept:C0010762 | lld:lifeskim |
pubmed-article:8786558 | lifeskim:mentions | umls-concept:C0021079 | lld:lifeskim |
pubmed-article:8786558 | lifeskim:mentions | umls-concept:C0332157 | lld:lifeskim |
pubmed-article:8786558 | lifeskim:mentions | umls-concept:C0205178 | lld:lifeskim |
pubmed-article:8786558 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:8786558 | lifeskim:mentions | umls-concept:C0851827 | lld:lifeskim |
pubmed-article:8786558 | lifeskim:mentions | umls-concept:C1701901 | lld:lifeskim |
pubmed-article:8786558 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:8786558 | pubmed:dateCreated | 1996-9-20 | lld:pubmed |
pubmed-article:8786558 | pubmed:abstractText | The primary objective of this paper was to characterize the role of metabolism in immunosuppression by acute exposure to cocaine. beta-Ionone has been used to study the role of metabolism in hepatotoxicity associated with acute exposure to cocaine, and was shown to produce a greater effect than other cytochrome P-450 (P-450) inducers. When beta-ionone (600 mg/kg s.c.) was pretreated 72 and 48 hr before the acute administration of cocaine (30 mg/kg i.p.) in B6C3F1 female mice, the antibody response to sheep red blood cells was significantly suppressed. Exposure to cocaine alone produced little or no suppression. The immunosuppression in cocaine + beta-ionone-treated mice was accompanied by a decrease in thymus weight and an increase in liver weight. Administration of metyrapone (40 mg/kg i.p.) 30 min before cocaine administration (40 mg/kg) blocked completely the suppression of the antibody response by cocaine in beta-ionone-pretreated mice. The reversal by metyrapone was additional evidence that a P-450 pathway was the critical metabolic pathway of cocaine to be immunosuppressive, and the inhibitory effect of metyrapone on cocaine N-demethylase was confirmed in liver microsomes. The inductive effects of beta-ionone were also characterized further. Cocaine N-demethylase activity was significantly induced by beta-ionone. The induction of P-450IIB1/2, the only isozyme shown previously to be associated with the hepatotoxicity by cocaine, was demonstrated by Western immunoblotting to be induced by beta-ionone at doses as low as 300 mg/kg; but was less than the induction associated with phenobarbital. Studies confirmed that acute exposure to cocaine also was immunosuppressive in phenobarbital-pretreated mice. Taken together, our present results suggest that the immunosuppression by acute exposure to cocaine is associated with the increased metabolism of cocaine to toxic metabolites by P-450, probably P-450IIB1/2, as demonstrated previously for its hepatotoxicity. | lld:pubmed |
pubmed-article:8786558 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8786558 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8786558 | pubmed:language | eng | lld:pubmed |
pubmed-article:8786558 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8786558 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8786558 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8786558 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8786558 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8786558 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8786558 | pubmed:month | Mar | lld:pubmed |
pubmed-article:8786558 | pubmed:issn | 0022-3565 | lld:pubmed |
pubmed-article:8786558 | pubmed:author | pubmed-author:HolsappleM... | lld:pubmed |
pubmed-article:8786558 | pubmed:author | pubmed-author:ParkS SSS | lld:pubmed |
pubmed-article:8786558 | pubmed:author | pubmed-author:JeongT CTC | lld:pubmed |
pubmed-article:8786558 | pubmed:author | pubmed-author:JordanS DSD | lld:pubmed |
pubmed-article:8786558 | pubmed:author | pubmed-author:MatulkaR ARA | lld:pubmed |
pubmed-article:8786558 | pubmed:author | pubmed-author:StanulisE DED | lld:pubmed |
pubmed-article:8786558 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8786558 | pubmed:volume | 276 | lld:pubmed |
pubmed-article:8786558 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8786558 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8786558 | pubmed:pagination | 1257-65 | lld:pubmed |
pubmed-article:8786558 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
pubmed-article:8786558 | pubmed:meshHeading | pubmed-meshheading:8786558-... | lld:pubmed |
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pubmed-article:8786558 | pubmed:meshHeading | pubmed-meshheading:8786558-... | lld:pubmed |
pubmed-article:8786558 | pubmed:year | 1996 | lld:pubmed |
pubmed-article:8786558 | pubmed:articleTitle | Immunosuppression induced by acute exposure to cocaine is dependent on metabolism by cytochrome P-450. | lld:pubmed |
pubmed-article:8786558 | pubmed:affiliation | Department of Pharmacology and Toxicology, Medical College of Virginia/Virginia Commonwealth University, Richmond, USA. | lld:pubmed |
pubmed-article:8786558 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8786558 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8786558 | lld:pubmed |