ChloroquineV1, PubMed, Corpus, bibRecord, 000563

Metallothionein induction by nonsteroidal antiinflammatory drugs.

Identifieur interne : 000563 ( PubMed/Corpus ); précédent : 000562; suivant : 000564

Metallothionein induction by nonsteroidal antiinflammatory drugs.

Auteurs : K H Summer ; D. Klein ; N. De Ruiter ; J. Abel

Source :

Biological trace element research [ 0163-4984 ]

RBID : pubmed:2484582

English descriptors

KwdEn :
- Animals, Anti-Inflammatory Agents, Non-Steroidal (pharmacology), Female, Immunoblotting, Kidney (drug effects), Kidney (metabolism), Liver (drug effects), Liver (metabolism), Lung (drug effects), Lung (metabolism), Metallothionein (biosynthesis), Metallothionein (genetics), Mice, Mice, Inbred C57BL, RNA, Messenger (biosynthesis).
MESH :
- chemical , biosynthesis : Metallothionein, RNA, Messenger.
- chemical , genetics : Metallothionein.
- chemical , pharmacology : Anti-Inflammatory Agents, Non-Steroidal.
- drug effects : Kidney, Liver, Lung.
- metabolism : Kidney, Liver, Lung.
- Animals, Female, Immunoblotting, Mice, Mice, Inbred C57BL.

Abstract

In the present study we report on the effects of commonly used nonsteroidal antiinflammatory drugs on metallothionein (MT) and MT-I mRNA levels. A single dose of chloroquine (100 mg/kg), diclofenac (100 mg/kg), indomethacin (10 mg/kg), or piroxicam (100 mg/kg) was administered ip to C57B1 mice. After 18 h, MT levels were determined with a Cd-saturation radioassay. MT-I mRNA levels were measured by Northern Blot analyses using a probe containing the mouse MT-I gene. All drugs tested caused an increase in the MT content of the liver but not of the kidneys and lung. The lowest and highest effects were observed with chloroquine (8 times the control value) and diclofenac (18 times), respectively. In accordance with the stimulation of MT synthesis, increased accumulation of hepatic MT-I mRNA could be demonstrated. These results indicate that elevated MT levels may contribute to the effectiveness of nonsteroidal antiinflammatory drugs in the treatment of rheumatoid arthritis (RA).

DOI: 10.1007/bf02917248
PubMed: 2484582

Links to Exploration step

pubmed:2484582

Le document en format XML

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<author><name sortKey="Summer, K H" sort="Summer, K H" uniqKey="Summer K" first="K H" last="Summer">K H Summer</name>
<affiliation><nlm:affiliation>Institute of Toxicology, Gesellschaft für Strahlen- und Umweltforschung München, Neuherberg, FRG.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Klein, D" sort="Klein, D" uniqKey="Klein D" first="D" last="Klein">D. Klein</name>
</author>
<author><name sortKey="De Ruiter, N" sort="De Ruiter, N" uniqKey="De Ruiter N" first="N" last="De Ruiter">N. De Ruiter</name>
</author>
<author><name sortKey="Abel, J" sort="Abel, J" uniqKey="Abel J" first="J" last="Abel">J. Abel</name>
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<date when="????"><PubDate><MedlineDate>1989 Jul-Sep</MedlineDate>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Metallothionein induction by nonsteroidal antiinflammatory drugs.</title>
<author><name sortKey="Summer, K H" sort="Summer, K H" uniqKey="Summer K" first="K H" last="Summer">K H Summer</name>
<affiliation><nlm:affiliation>Institute of Toxicology, Gesellschaft für Strahlen- und Umweltforschung München, Neuherberg, FRG.</nlm:affiliation>
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<author><name sortKey="Klein, D" sort="Klein, D" uniqKey="Klein D" first="D" last="Klein">D. Klein</name>
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<author><name sortKey="De Ruiter, N" sort="De Ruiter, N" uniqKey="De Ruiter N" first="N" last="De Ruiter">N. De Ruiter</name>
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<author><name sortKey="Abel, J" sort="Abel, J" uniqKey="Abel J" first="J" last="Abel">J. Abel</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Anti-Inflammatory Agents, Non-Steroidal (pharmacology)</term>
<term>Female</term>
<term>Immunoblotting</term>
<term>Kidney (drug effects)</term>
<term>Kidney (metabolism)</term>
<term>Liver (drug effects)</term>
<term>Liver (metabolism)</term>
<term>Lung (drug effects)</term>
<term>Lung (metabolism)</term>
<term>Metallothionein (biosynthesis)</term>
<term>Metallothionein (genetics)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>RNA, Messenger (biosynthesis)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Metallothionein</term>
<term>RNA, Messenger</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Metallothionein</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Kidney</term>
<term>Liver</term>
<term>Lung</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Kidney</term>
<term>Liver</term>
<term>Lung</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Female</term>
<term>Immunoblotting</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
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<front><div type="abstract" xml:lang="en">In the present study we report on the effects of commonly used nonsteroidal antiinflammatory drugs on metallothionein (MT) and MT-I mRNA levels. A single dose of chloroquine (100 mg/kg), diclofenac (100 mg/kg), indomethacin (10 mg/kg), or piroxicam (100 mg/kg) was administered ip to C57B1 mice. After 18 h, MT levels were determined with a Cd-saturation radioassay. MT-I mRNA levels were measured by Northern Blot analyses using a probe containing the mouse MT-I gene. All drugs tested caused an increase in the MT content of the liver but not of the kidneys and lung. The lowest and highest effects were observed with chloroquine (8 times the control value) and diclofenac (18 times), respectively. In accordance with the stimulation of MT synthesis, increased accumulation of hepatic MT-I mRNA could be demonstrated. These results indicate that elevated MT levels may contribute to the effectiveness of nonsteroidal antiinflammatory drugs in the treatment of rheumatoid arthritis (RA).</div>
</front>
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<Month>11</Month>
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<DateRevised><Year>2019</Year>
<Month>10</Month>
<Day>22</Day>
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<JournalIssue CitedMedium="Print"><Volume>21</Volume>
<PubDate><MedlineDate>1989 Jul-Sep</MedlineDate>
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<Title>Biological trace element research</Title>
<ISOAbbreviation>Biol Trace Elem Res</ISOAbbreviation>
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<ArticleTitle>Metallothionein induction by nonsteroidal antiinflammatory drugs.</ArticleTitle>
<Pagination><MedlinePgn>165-9</MedlinePgn>
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<Abstract><AbstractText>In the present study we report on the effects of commonly used nonsteroidal antiinflammatory drugs on metallothionein (MT) and MT-I mRNA levels. A single dose of chloroquine (100 mg/kg), diclofenac (100 mg/kg), indomethacin (10 mg/kg), or piroxicam (100 mg/kg) was administered ip to C57B1 mice. After 18 h, MT levels were determined with a Cd-saturation radioassay. MT-I mRNA levels were measured by Northern Blot analyses using a probe containing the mouse MT-I gene. All drugs tested caused an increase in the MT content of the liver but not of the kidneys and lung. The lowest and highest effects were observed with chloroquine (8 times the control value) and diclofenac (18 times), respectively. In accordance with the stimulation of MT synthesis, increased accumulation of hepatic MT-I mRNA could be demonstrated. These results indicate that elevated MT levels may contribute to the effectiveness of nonsteroidal antiinflammatory drugs in the treatment of rheumatoid arthritis (RA).</AbstractText>
</Abstract>
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<ForeName>K H</ForeName>
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<AffiliationInfo><Affiliation>Institute of Toxicology, Gesellschaft für Strahlen- und Umweltforschung München, Neuherberg, FRG.</Affiliation>
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<Language>eng</Language>
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<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
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<MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName>
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<MeshHeading><DescriptorName UI="D008668" MajorTopicYN="N">Metallothionein</DescriptorName>
<QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName>
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Metallothionein induction by nonsteroidal antiinflammatory drugs.

Metallothionein induction by nonsteroidal antiinflammatory drugs.

Source :

English descriptors

Abstract

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