Lens opacities associated with lipidosis-like ultrastructural alterations in rats treated with chloroquine, chlorphentermine, or iprindole
Identifieur interne : 000981 ( Istex/Corpus ); précédent : 000980; suivant : 000982Lens opacities associated with lipidosis-like ultrastructural alterations in rats treated with chloroquine, chlorphentermine, or iprindole
Auteurs : Detlev Drenckhahn ; Renate Lüllmann-RauchSource :
- Experimental Eye Research [ 0014-4835 ] ; 1977.
English descriptors
- Teeft :
- Abnormal inclusions, Amphiphilic, Anorectic drug, Anterior, Anterior lens, Anterior lens surface, Anterior sutures, Broekhuyse, Cataract, Chloroquine, Chlorphentermine, Control animals, Cortical lens cells, Cytoplasmic, Degeneration, Diffuse subcapsular opacities, Drenckhahn, Drug treatment, Epithelial, Epithelial cells, Epithelium, Inclusion, Iprindole, Lamellated, Lens, Lens cells, Lens epithelium, Lens opacities, Lenticular, Lenticular alterations, Lipid, Ocular pathology, Opacity, Phentermine, Polar lipids, Posterior cortex, Present study, Subcapsular, Subcapsular opacities, Sutural, Suture, Ultrastructural, Ultrastructural alterations, Vacuole, Wassermann, Whole lenses.
Abstract
Abstract: The present study deals with the effects, upon transparency and cellular structure of rat lenses of three amphiphilic cationic drugs (chloroquine, chlorphentermine, iprindole) which were previously shown to induce generalized lipidosis. Within 6 weeks of treatment with high doses of any of the drugs, conspicuous biomicroscopic changes occurred in all lenses. They were characterized (a) by diffuse subcapsular opacities which were most prominent in the anterior part of the lens, and (b) by prominent anterior and posterior sutural opacities. The morphological alterations consisted of: accumulation of abnormal lamellated inclusions in the cytoplasm of epithelial cells and cortical lens cells; proliferation of the lens epithelium; degeneration of superficial cortical lens cells. The present ultrastructural findings in lens epithelium are reminiscent of lens alterations found in inherited lipidoses of humans. The subcapsular opacities are proposed to result from light scattering due to the presence of numerous abnormal cytoplasmic inclusions. The sutural opacities are attributed to epithelial proliferation along the anterior sutures and to degeneration of the anterior and posterior sutural endings of the superficial cortical lens cells. The lamellated cytoplasmic inclusions are thought to reflect intracellular accumulation of non-digestible polar lipids due to drug-impaired lipid catabolism. Degeneration of the superficial cortical lens cells is tentatively explained also to result from disturbance of polar lipid metabolism in the lens affecting mainly those lens cells that were growing during the period of drug treatment.
Url:
DOI: 10.1016/0014-4835(77)90120-8
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ISTEX:52ABB3089AC704692679B1A7503885C7FE592B94Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Lens opacities associated with lipidosis-like ultrastructural alterations in rats treated with chloroquine, chlorphentermine, or iprindole</title><author><name sortKey="Drenckhahn, Detlev" sort="Drenckhahn, Detlev" uniqKey="Drenckhahn D" first="Detlev" last="Drenckhahn">Detlev Drenckhahn</name><affiliation><mods:affiliation>Department of Anatomy, University of Kiel, Kiel, West Germany</mods:affiliation></affiliation></author><author><name sortKey="Lullmann Rauch, Renate" sort="Lullmann Rauch, Renate" uniqKey="Lullmann Rauch R" first="Renate" last="Lüllmann-Rauch">Renate Lüllmann-Rauch</name><affiliation><mods:affiliation>Department of Anatomy, University of Kiel, Kiel, West Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:52ABB3089AC704692679B1A7503885C7FE592B94</idno><date when="1977" year="1977">1977</date><idno type="doi">10.1016/0014-4835(77)90120-8</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-86Q36B3B-S/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000981</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000981</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Lens opacities associated with lipidosis-like ultrastructural alterations in rats treated with chloroquine, chlorphentermine, or iprindole</title><author><name sortKey="Drenckhahn, Detlev" sort="Drenckhahn, Detlev" uniqKey="Drenckhahn D" first="Detlev" last="Drenckhahn">Detlev Drenckhahn</name><affiliation><mods:affiliation>Department of Anatomy, University of Kiel, Kiel, West Germany</mods:affiliation></affiliation></author><author><name sortKey="Lullmann Rauch, Renate" sort="Lullmann Rauch, Renate" uniqKey="Lullmann Rauch R" first="Renate" last="Lüllmann-Rauch">Renate Lüllmann-Rauch</name><affiliation><mods:affiliation>Department of Anatomy, University of Kiel, Kiel, West Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Experimental Eye Research</title><title level="j" type="abbrev">YEXER</title><idno type="ISSN">0014-4835</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1977">1977</date><biblScope unit="volume">24</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="621">621</biblScope><biblScope unit="page" to="632">632</biblScope></imprint><idno type="ISSN">0014-4835</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0014-4835</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Abnormal inclusions</term><term>Amphiphilic</term><term>Anorectic drug</term><term>Anterior</term><term>Anterior lens</term><term>Anterior lens surface</term><term>Anterior sutures</term><term>Broekhuyse</term><term>Cataract</term><term>Chloroquine</term><term>Chlorphentermine</term><term>Control animals</term><term>Cortical lens cells</term><term>Cytoplasmic</term><term>Degeneration</term><term>Diffuse subcapsular opacities</term><term>Drenckhahn</term><term>Drug treatment</term><term>Epithelial</term><term>Epithelial cells</term><term>Epithelium</term><term>Inclusion</term><term>Iprindole</term><term>Lamellated</term><term>Lens</term><term>Lens cells</term><term>Lens epithelium</term><term>Lens opacities</term><term>Lenticular</term><term>Lenticular alterations</term><term>Lipid</term><term>Ocular pathology</term><term>Opacity</term><term>Phentermine</term><term>Polar lipids</term><term>Posterior cortex</term><term>Present study</term><term>Subcapsular</term><term>Subcapsular opacities</term><term>Sutural</term><term>Suture</term><term>Ultrastructural</term><term>Ultrastructural alterations</term><term>Vacuole</term><term>Wassermann</term><term>Whole lenses</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The present study deals with the effects, upon transparency and cellular structure of rat lenses of three amphiphilic cationic drugs (chloroquine, chlorphentermine, iprindole) which were previously shown to induce generalized lipidosis. Within 6 weeks of treatment with high doses of any of the drugs, conspicuous biomicroscopic changes occurred in all lenses. They were characterized (a) by diffuse subcapsular opacities which were most prominent in the anterior part of the lens, and (b) by prominent anterior and posterior sutural opacities. The morphological alterations consisted of: accumulation of abnormal lamellated inclusions in the cytoplasm of epithelial cells and cortical lens cells; proliferation of the lens epithelium; degeneration of superficial cortical lens cells. The present ultrastructural findings in lens epithelium are reminiscent of lens alterations found in inherited lipidoses of humans. The subcapsular opacities are proposed to result from light scattering due to the presence of numerous abnormal cytoplasmic inclusions. The sutural opacities are attributed to epithelial proliferation along the anterior sutures and to degeneration of the anterior and posterior sutural endings of the superficial cortical lens cells. The lamellated cytoplasmic inclusions are thought to reflect intracellular accumulation of non-digestible polar lipids due to drug-impaired lipid catabolism. Degeneration of the superficial cortical lens cells is tentatively explained also to result from disturbance of polar lipid metabolism in the lens affecting mainly those lens cells that were growing during the period of drug treatment.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>opacity</json:string><json:string>lipid</json:string><json:string>chloroquine</json:string><json:string>chlorphentermine</json:string><json:string>subcapsular</json:string><json:string>cataract</json:string><json:string>epithelium</json:string><json:string>iprindole</json:string><json:string>lens cells</json:string><json:string>epithelial</json:string><json:string>cytoplasmic</json:string><json:string>phentermine</json:string><json:string>lamellated</json:string><json:string>suture</json:string><json:string>lens epithelium</json:string><json:string>broekhuyse</json:string><json:string>drenckhahn</json:string><json:string>sutural</json:string><json:string>wassermann</json:string><json:string>epithelial cells</json:string><json:string>amphiphilic</json:string><json:string>ultrastructural</json:string><json:string>cortical lens cells</json:string><json:string>lenticular</json:string><json:string>vacuole</json:string><json:string>diffuse subcapsular opacities</json:string><json:string>anterior sutures</json:string><json:string>polar lipids</json:string><json:string>abnormal inclusions</json:string><json:string>degeneration</json:string><json:string>drug treatment</json:string><json:string>subcapsular opacities</json:string><json:string>lens opacities</json:string><json:string>present study</json:string><json:string>anorectic drug</json:string><json:string>lens</json:string><json:string>inclusion</json:string><json:string>anterior lens</json:string><json:string>anterior lens surface</json:string><json:string>whole lenses</json:string><json:string>control animals</json:string><json:string>ultrastructural alterations</json:string><json:string>posterior cortex</json:string><json:string>lenticular alterations</json:string><json:string>ocular pathology</json:string><json:string>anterior</json:string></teeft></keywords><author><json:item><name>Detlev Drenckhahn</name><affiliations><json:string>Department of Anatomy, University of Kiel, Kiel, West Germany</json:string></affiliations></json:item><json:item><name>Renate Lüllmann-Rauch</name><affiliations><json:string>Department of Anatomy, University of Kiel, Kiel, West Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>cataract</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>chloroquine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>chlorphentermine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>iprindole</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>lipidosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>drug-induced</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>rat</value></json:item></subject><arkIstex>ark:/67375/6H6-86Q36B3B-S</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: The present study deals with the effects, upon transparency and cellular structure of rat lenses of three amphiphilic cationic drugs (chloroquine, chlorphentermine, iprindole) which were previously shown to induce generalized lipidosis. Within 6 weeks of treatment with high doses of any of the drugs, conspicuous biomicroscopic changes occurred in all lenses. They were characterized (a) by diffuse subcapsular opacities which were most prominent in the anterior part of the lens, and (b) by prominent anterior and posterior sutural opacities. The morphological alterations consisted of: accumulation of abnormal lamellated inclusions in the cytoplasm of epithelial cells and cortical lens cells; proliferation of the lens epithelium; degeneration of superficial cortical lens cells. The present ultrastructural findings in lens epithelium are reminiscent of lens alterations found in inherited lipidoses of humans. The subcapsular opacities are proposed to result from light scattering due to the presence of numerous abnormal cytoplasmic inclusions. The sutural opacities are attributed to epithelial proliferation along the anterior sutures and to degeneration of the anterior and posterior sutural endings of the superficial cortical lens cells. The lamellated cytoplasmic inclusions are thought to reflect intracellular accumulation of non-digestible polar lipids due to drug-impaired lipid catabolism. Degeneration of the superficial cortical lens cells is tentatively explained also to result from disturbance of polar lipid metabolism in the lens affecting mainly those lens cells that were growing during the period of drug treatment.</abstract><qualityIndicators><refBibsNative>true</refBibsNative><abstractWordCount>231</abstractWordCount><abstractCharCount>1654</abstractCharCount><keywordCount>7</keywordCount><score>7.782</score><pdfWordCount>3010</pdfWordCount><pdfCharCount>24704</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>12</pdfPageCount><pdfPageSize>491.12 x 704.84 pts</pdfPageSize></qualityIndicators><title>Lens opacities associated with lipidosis-like ultrastructural alterations in rats treated with chloroquine, chlorphentermine, or iprindole</title><pmid><json:string>872905</json:string></pmid><pii><json:string>0014-4835(77)90120-8</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>The Human Lens in Relation to Cataract</title><language><json:string>unknown</json:string></language><pages><first>135</first><last>144</last></pages></serie><host><title>Experimental Eye Research</title><language><json:string>unknown</json:string></language><publicationDate>1977</publicationDate><issn><json:string>0014-4835</json:string></issn><pii><json:string>S0014-4835(00)X0179-0</json:string></pii><volume>24</volume><issue>6</issue><pages><first>621</first><last>632</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1s</json:string><json:string>1977</json:string><json:string>11s</json:string></date><geogName></geogName><orgName><json:string>Biochem</json:string><json:string>Deutsche Forschungsgemeinschaft</json:string></orgName><orgName_funder><json:string>Deutsche Forschungsgemeinschaft</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Professor Dr</json:string><json:string>J. Pathol</json:string><json:string>W. de Decker</json:string><json:string>J. Ophthnlmol</json:string><json:string>I. Interaction</json:string><json:string>J. 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Broekhuyse and Veerkamp, 1973</json:string><json:string>Seydel and Wassermann, 1973</json:string><json:string>Robb and Kuwabara, 1973</json:string><json:string>Broekhuyse, 1974</json:string><json:string>Abraham and Hendy, 1970</json:string><json:string>Hogan, Alvarado and Weddell, 1971</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-86Q36B3B-S</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - ophthalmology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - ophthalmology & optometry</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Neuroscience</json:string><json:string>3 - Cellular and Molecular Neuroscience</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Neuroscience</json:string><json:string>3 - Sensory Systems</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Ophthalmology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string><json:string>4 - maladies metaboliques</json:string></inist></categories><publicationDate>1977</publicationDate><copyrightDate>1977</copyrightDate><doi><json:string>10.1016/0014-4835(77)90120-8</json:string></doi><id>52ABB3089AC704692679B1A7503885C7FE592B94</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-86Q36B3B-S/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-86Q36B3B-S/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-86Q36B3B-S/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">Lens opacities associated with lipidosis-like ultrastructural alterations in rats treated with chloroquine, chlorphentermine, or iprindole</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>elsevier</p></licence></availability><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M"></p><date>1977</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Lens opacities associated with lipidosis-like ultrastructural alterations in rats treated with chloroquine, chlorphentermine, or iprindole</title><author xml:id="author-0000"><persName><forename type="first">Detlev</forename><surname>Drenckhahn</surname></persName><affiliation>Department of Anatomy, University of Kiel, Kiel, West Germany</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Renate</forename><surname>Lüllmann-Rauch</surname></persName><affiliation>Department of Anatomy, University of Kiel, Kiel, West Germany</affiliation></author><idno type="istex">52ABB3089AC704692679B1A7503885C7FE592B94</idno><idno type="ark">ark:/67375/6H6-86Q36B3B-S</idno><idno type="DOI">10.1016/0014-4835(77)90120-8</idno><idno type="PII">0014-4835(77)90120-8</idno></analytic><monogr><title level="j">Experimental Eye Research</title><title level="j" type="abbrev">YEXER</title><idno type="pISSN">0014-4835</idno><idno type="PII">S0014-4835(00)X0179-0</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1977"></date><biblScope unit="volume">24</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="621">621</biblScope><biblScope unit="page" to="632">632</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1977</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: The present study deals with the effects, upon transparency and cellular structure of rat lenses of three amphiphilic cationic drugs (chloroquine, chlorphentermine, iprindole) which were previously shown to induce generalized lipidosis. Within 6 weeks of treatment with high doses of any of the drugs, conspicuous biomicroscopic changes occurred in all lenses. They were characterized (a) by diffuse subcapsular opacities which were most prominent in the anterior part of the lens, and (b) by prominent anterior and posterior sutural opacities. The morphological alterations consisted of: accumulation of abnormal lamellated inclusions in the cytoplasm of epithelial cells and cortical lens cells; proliferation of the lens epithelium; degeneration of superficial cortical lens cells. The present ultrastructural findings in lens epithelium are reminiscent of lens alterations found in inherited lipidoses of humans. The subcapsular opacities are proposed to result from light scattering due to the presence of numerous abnormal cytoplasmic inclusions. The sutural opacities are attributed to epithelial proliferation along the anterior sutures and to degeneration of the anterior and posterior sutural endings of the superficial cortical lens cells. The lamellated cytoplasmic inclusions are thought to reflect intracellular accumulation of non-digestible polar lipids due to drug-impaired lipid catabolism. Degeneration of the superficial cortical lens cells is tentatively explained also to result from disturbance of polar lipid metabolism in the lens affecting mainly those lens cells that were growing during the period of drug treatment.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>cataract</term></item><item><term>chloroquine</term></item><item><term>chlorphentermine</term></item><item><term>iprindole</term></item><item><term>lipidosis</term></item><item><term>drug-induced</term></item><item><term>rat</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1976-09-27">Modified</change><change when="1977">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-86Q36B3B-S/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>YEXER</jid><aid>77901208</aid><ce:pii>0014-4835(77)90120-8</ce:pii><ce:doi>10.1016/0014-4835(77)90120-8</ce:doi><ce:copyright type="unknown" year="1977"></ce:copyright></item-info><head><ce:title>Lens opacities associated with lipidosis-like ultrastructural alterations in rats treated with chloroquine, chlorphentermine, or iprindole</ce:title><ce:author-group><ce:author><ce:given-name>Detlev</ce:given-name><ce:surname>Drenckhahn</ce:surname></ce:author><ce:author><ce:given-name>Renate</ce:given-name><ce:surname>Lüllmann-Rauch</ce:surname></ce:author><ce:affiliation><ce:textfn>Department of Anatomy, University of Kiel, Kiel, West Germany</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="13" month="7" year="1976"></ce:date-received><ce:date-revised day="27" month="9" year="1976"></ce:date-revised><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The present study deals with the effects, upon transparency and cellular structure of rat lenses of three amphiphilic cationic drugs (chloroquine, chlorphentermine, iprindole) which were previously shown to induce generalized lipidosis. Within 6 weeks of treatment with high doses of any of the drugs, conspicuous biomicroscopic changes occurred in all lenses. They were characterized (a) by diffuse subcapsular opacities which were most prominent in the anterior part of the lens, and (b) by prominent anterior and posterior sutural opacities. The morphological alterations consisted of: accumulation of abnormal lamellated inclusions in the cytoplasm of epithelial cells and cortical lens cells; proliferation of the lens epithelium; degeneration of superficial cortical lens cells. The present ultrastructural findings in lens epithelium are reminiscent of lens alterations found in inherited lipidoses of humans. The subcapsular opacities are proposed to result from light scattering due to the presence of numerous abnormal cytoplasmic inclusions. The sutural opacities are attributed to epithelial proliferation along the anterior sutures and to degeneration of the anterior and posterior sutural endings of the superficial cortical lens cells.</ce:simple-para><ce:simple-para>The lamellated cytoplasmic inclusions are thought to reflect intracellular accumulation of non-digestible polar lipids due to drug-impaired lipid catabolism. Degeneration of the superficial cortical lens cells is tentatively explained also to result from disturbance of polar lipid metabolism in the lens affecting mainly those lens cells that were growing during the period of drug treatment.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>cataract</ce:text></ce:keyword><ce:keyword><ce:text>chloroquine</ce:text></ce:keyword><ce:keyword><ce:text>chlorphentermine</ce:text></ce:keyword><ce:keyword><ce:text>iprindole</ce:text></ce:keyword><ce:keyword><ce:text>lipidosis</ce:text></ce:keyword><ce:keyword><ce:text>drug-induced</ce:text></ce:keyword><ce:keyword><ce:text>rat</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Lens opacities associated with lipidosis-like ultrastructural alterations in rats treated with chloroquine, chlorphentermine, or iprindole</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Lens opacities associated with lipidosis-like ultrastructural alterations in rats treated with chloroquine, chlorphentermine, or iprindole</title></titleInfo><name type="personal"><namePart type="given">Detlev</namePart><namePart type="family">Drenckhahn</namePart><affiliation>Department of Anatomy, University of Kiel, Kiel, West Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Renate</namePart><namePart type="family">Lüllmann-Rauch</namePart><affiliation>Department of Anatomy, University of Kiel, Kiel, West Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1977</dateIssued><dateModified encoding="w3cdtf">1976-09-27</dateModified><copyrightDate encoding="w3cdtf">1977</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: The present study deals with the effects, upon transparency and cellular structure of rat lenses of three amphiphilic cationic drugs (chloroquine, chlorphentermine, iprindole) which were previously shown to induce generalized lipidosis. Within 6 weeks of treatment with high doses of any of the drugs, conspicuous biomicroscopic changes occurred in all lenses. They were characterized (a) by diffuse subcapsular opacities which were most prominent in the anterior part of the lens, and (b) by prominent anterior and posterior sutural opacities. The morphological alterations consisted of: accumulation of abnormal lamellated inclusions in the cytoplasm of epithelial cells and cortical lens cells; proliferation of the lens epithelium; degeneration of superficial cortical lens cells. The present ultrastructural findings in lens epithelium are reminiscent of lens alterations found in inherited lipidoses of humans. The subcapsular opacities are proposed to result from light scattering due to the presence of numerous abnormal cytoplasmic inclusions. The sutural opacities are attributed to epithelial proliferation along the anterior sutures and to degeneration of the anterior and posterior sutural endings of the superficial cortical lens cells. The lamellated cytoplasmic inclusions are thought to reflect intracellular accumulation of non-digestible polar lipids due to drug-impaired lipid catabolism. Degeneration of the superficial cortical lens cells is tentatively explained also to result from disturbance of polar lipid metabolism in the lens affecting mainly those lens cells that were growing during the period of drug treatment.</abstract><subject><genre>Keywords</genre><topic>cataract</topic><topic>chloroquine</topic><topic>chlorphentermine</topic><topic>iprindole</topic><topic>lipidosis</topic><topic>drug-induced</topic><topic>rat</topic></subject><relatedItem type="host"><titleInfo><title>Experimental Eye Research</title></titleInfo><titleInfo type="abbreviated"><title>YEXER</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1977</dateIssued></originInfo><identifier type="ISSN">0014-4835</identifier><identifier type="PII">S0014-4835(00)X0179-0</identifier><part><date>1977</date><detail type="volume"><number>24</number><caption>vol.</caption></detail><detail type="issue"><number>6</number><caption>no.</caption></detail><extent unit="issue-pages"><start>537</start><end>639</end></extent><extent unit="pages"><start>621</start><end>632</end></extent></part></relatedItem><identifier type="istex">52ABB3089AC704692679B1A7503885C7FE592B94</identifier><identifier type="ark">ark:/67375/6H6-86Q36B3B-S</identifier><identifier type="DOI">10.1016/0014-4835(77)90120-8</identifier><identifier type="PII">0014-4835(77)90120-8</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-86Q36B3B-S/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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