Lens opacities associated with lipidosis-like ultrastructural alterations in rats treated with chloroquine, chlorphentermine, or iprindole
Identifieur interne : 003947 ( Main/Curation ); précédent : 003946; suivant : 003948Lens opacities associated with lipidosis-like ultrastructural alterations in rats treated with chloroquine, chlorphentermine, or iprindole
Auteurs : Detlev Drenckhahn [Allemagne] ; Renate Lüllmann-Rauch [Allemagne]Source :
- 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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<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>
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<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>
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