Influence of chloroquine and lidocaine on retention and cytotoxic effects of [131I]EGF: studies on cultured glioma cells.
Identifieur interne : 000551 ( PubMed/Corpus ); précédent : 000550; suivant : 000552Influence of chloroquine and lidocaine on retention and cytotoxic effects of [131I]EGF: studies on cultured glioma cells.
Auteurs : J. Capala ; J. CarlssonSource :
- International journal of radiation biology [ 0955-3002 ] ; 1991.
English descriptors
- KwdEn :
- MESH :
- chemical , pharmacokinetics : Epidermal Growth Factor.
- chemical , therapeutic use : Chloroquine, Epidermal Growth Factor, Iodine Radioisotopes, Lidocaine.
- radiotherapy : Glioma.
- Cells, Cultured, Humans.
Abstract
Targeting of toxic substances to the epidermal growth factor, EGF, receptor might be an attractive therapeutic approach because of the increased receptor-expression in some human tumours such as, for example, malignant gliomas and squamous lung carcinomas. Radiation effects of [131I]EGF on human malignant glioma cells growing as monolayers were analysed in this study. The cells were, in all cases, incubated for 25 min with about 350 kBq/ml [131I]EGF, which gave a total binding of 3.2-3.5 kBq/10(5) cells. The rapid release of activity from the cells caused by the normal degradation of EGF was inhibited by incubation with 30 microM chloroquine or 5 mM lidocaine added to the cell culture medium. These substances are, at these concentrations, known to inhibit proteolytic processes in lysosomes. No effects of the inhibitors alone were observed on cell growth and clonogenic survival. Inhibition of EGF degradation by chloroquine or lidocaine resulted in a significantly prolonged association of 131I with the test cells. About 70% of the initially bound radioactivity remained in the cells giving, after 6 h, a binding of 2.1-2.5 kBq/10(5) cells. A 6 h exposure to the radiation from 131I decays, mediated mainly by specifically bound EGF, gave a survival value of about 50%. Such an effect corresponds to a treatment of 2.5 Gy 60Co gamma-radiation. This is promising considering that, when monolayers are applied, only a very small fraction of the released energy from the 131I decays is deposited in the cells. Effects from non-receptor bound [131I]EGF were analysed after presaturation of the receptors with non-radioactive EGF, and gave no or very small changes in survival.
DOI: 10.1080/09553009114552341
PubMed: 1679089
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Carlsson</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1991">1991</date><idno type="RBID">pubmed:1679089</idno><idno type="pmid">1679089</idno><idno type="doi">10.1080/09553009114552341</idno><idno type="wicri:Area/PubMed/Corpus">000551</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000551</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Influence of chloroquine and lidocaine on retention and cytotoxic effects of [131I]EGF: studies on cultured glioma cells.</title><author><name sortKey="Capala, J" sort="Capala, J" uniqKey="Capala J" first="J" last="Capala">J. Capala</name><affiliation><nlm:affiliation>Department of Radiation Sciences, Uppsala University, Sweden.</nlm:affiliation></affiliation></author><author><name sortKey="Carlsson, J" sort="Carlsson, J" uniqKey="Carlsson J" first="J" last="Carlsson">J. Carlsson</name></author></analytic><series><title level="j">International journal of radiation biology</title><idno type="ISSN">0955-3002</idno><imprint><date when="1991" type="published">1991</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cells, Cultured</term><term>Chloroquine (therapeutic use)</term><term>Epidermal Growth Factor (pharmacokinetics)</term><term>Epidermal Growth Factor (therapeutic use)</term><term>Glioma (radiotherapy)</term><term>Humans</term><term>Iodine Radioisotopes (therapeutic use)</term><term>Lidocaine (therapeutic use)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Epidermal Growth Factor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Chloroquine</term><term>Epidermal Growth Factor</term><term>Iodine Radioisotopes</term><term>Lidocaine</term></keywords><keywords scheme="MESH" qualifier="radiotherapy" xml:lang="en"><term>Glioma</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cells, Cultured</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Targeting of toxic substances to the epidermal growth factor, EGF, receptor might be an attractive therapeutic approach because of the increased receptor-expression in some human tumours such as, for example, malignant gliomas and squamous lung carcinomas. Radiation effects of [131I]EGF on human malignant glioma cells growing as monolayers were analysed in this study. The cells were, in all cases, incubated for 25 min with about 350 kBq/ml [131I]EGF, which gave a total binding of 3.2-3.5 kBq/10(5) cells. The rapid release of activity from the cells caused by the normal degradation of EGF was inhibited by incubation with 30 microM chloroquine or 5 mM lidocaine added to the cell culture medium. These substances are, at these concentrations, known to inhibit proteolytic processes in lysosomes. No effects of the inhibitors alone were observed on cell growth and clonogenic survival. Inhibition of EGF degradation by chloroquine or lidocaine resulted in a significantly prolonged association of 131I with the test cells. About 70% of the initially bound radioactivity remained in the cells giving, after 6 h, a binding of 2.1-2.5 kBq/10(5) cells. A 6 h exposure to the radiation from 131I decays, mediated mainly by specifically bound EGF, gave a survival value of about 50%. Such an effect corresponds to a treatment of 2.5 Gy 60Co gamma-radiation. This is promising considering that, when monolayers are applied, only a very small fraction of the released energy from the 131I decays is deposited in the cells. Effects from non-receptor bound [131I]EGF were analysed after presaturation of the receptors with non-radioactive EGF, and gave no or very small changes in survival.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1679089</PMID><DateCompleted><Year>1991</Year><Month>10</Month><Day>03</Day></DateCompleted><DateRevised><Year>2019</Year><Month>09</Month><Day>07</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0955-3002</ISSN><JournalIssue CitedMedium="Print"><Volume>60</Volume><Issue>3</Issue><PubDate><Year>1991</Year><Month>Sep</Month></PubDate></JournalIssue><Title>International journal of radiation biology</Title><ISOAbbreviation>Int. J. Radiat. Biol.</ISOAbbreviation></Journal><ArticleTitle>Influence of chloroquine and lidocaine on retention and cytotoxic effects of [131I]EGF: studies on cultured glioma cells.</ArticleTitle><Pagination><MedlinePgn>497-510</MedlinePgn></Pagination><Abstract><AbstractText>Targeting of toxic substances to the epidermal growth factor, EGF, receptor might be an attractive therapeutic approach because of the increased receptor-expression in some human tumours such as, for example, malignant gliomas and squamous lung carcinomas. Radiation effects of [131I]EGF on human malignant glioma cells growing as monolayers were analysed in this study. The cells were, in all cases, incubated for 25 min with about 350 kBq/ml [131I]EGF, which gave a total binding of 3.2-3.5 kBq/10(5) cells. The rapid release of activity from the cells caused by the normal degradation of EGF was inhibited by incubation with 30 microM chloroquine or 5 mM lidocaine added to the cell culture medium. These substances are, at these concentrations, known to inhibit proteolytic processes in lysosomes. No effects of the inhibitors alone were observed on cell growth and clonogenic survival. Inhibition of EGF degradation by chloroquine or lidocaine resulted in a significantly prolonged association of 131I with the test cells. About 70% of the initially bound radioactivity remained in the cells giving, after 6 h, a binding of 2.1-2.5 kBq/10(5) cells. A 6 h exposure to the radiation from 131I decays, mediated mainly by specifically bound EGF, gave a survival value of about 50%. Such an effect corresponds to a treatment of 2.5 Gy 60Co gamma-radiation. This is promising considering that, when monolayers are applied, only a very small fraction of the released energy from the 131I decays is deposited in the cells. Effects from non-receptor bound [131I]EGF were analysed after presaturation of the receptors with non-radioactive EGF, and gave no or very small changes in survival.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Capala</LastName><ForeName>J</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Radiation Sciences, Uppsala University, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carlsson</LastName><ForeName>J</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Int J Radiat Biol</MedlineTA><NlmUniqueID>8809243</NlmUniqueID><ISSNLinking>0955-3002</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007457">Iodine Radioisotopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>62229-50-9</RegistryNumber><NameOfSubstance UI="D004815">Epidermal Growth Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>98PI200987</RegistryNumber><NameOfSubstance UI="D008012">Lidocaine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CitationSubset>S</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004815" MajorTopicYN="N">Epidermal Growth Factor</DescriptorName><QualifierName UI="Q000493" MajorTopicYN="Y">pharmacokinetics</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005910" MajorTopicYN="N">Glioma</DescriptorName><QualifierName UI="Q000532" MajorTopicYN="Y">radiotherapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007457" MajorTopicYN="N">Iodine Radioisotopes</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008012" MajorTopicYN="N">Lidocaine</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1991</Year><Month>9</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1991</Year><Month>9</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1991</Year><Month>9</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1679089</ArticleId><ArticleId IdType="pii">EYNRJR895PVYC0R4</ArticleId><ArticleId IdType="doi">10.1080/09553009114552341</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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