Tamoxifen-induced generalized lipidosis in rats subchronically treated with high doses
Identifieur interne : 003759 ( Main/Exploration ); précédent : 003758; suivant : 003760Tamoxifen-induced generalized lipidosis in rats subchronically treated with high doses
Auteurs : Heinz Lüllmann [Allemagne] ; Renate Lüllmann-Rauch [Allemagne]Source :
- Toxicology and Applied Pharmacology [ 0041-008X ] ; 1981.
English descriptors
- Teeft :
- Abnormal, Abnormal cells, Abnormal inclusions, Adjacent stripe, Adrenal, Adrenal cortex, Adrenal gland, Adrenocortical, Adrenocortical cells, Amphiphilic, Amphiphilic cationic compounds, Amphiphilic cationic drugs, Araldite, Araldite section, Arrows point, Breast cancer, Cationic, Cationic drugs, Clinical application, Control rats, Cornea1 opacities, Crista type, Cytoplasmic inclusions, Electron microscopy, Experimental animals, Fasciculata, Fasciculata cells, Foam alveolar macrophages, Food consumption, General architecture, Generalized lipidosis, Ground chow, Higher magnification, Inclusion, Intercellular contacts, Lamellar, Lamellar inclusions, Light microscopy, Lipidosis, Lymph node, Nucleus supraopticus, Polar lipids, Present findings, Rat, Rats subchronically, Reticularis, Retinal pigment epithelium, Side chain, Soleus muscle, Tamoxifen, Tamoxifen citrate, Transitional types, Tubular type, Zona, Zona fasciculata, Zona reticularis.
Abstract
Abstract: The antiestrogenic drug tamoxifen is an amphiphilic cationic compound and might therefore be suspected to interfere with intralysosomal catabolism of polar lipids as previously observed with several other amphiphilic cationic drugs. Large oral doses (100–130 mg/kg) of tamoxifen were administered to rats for 6 to 14 weeks. Tissues including liver, lung, lymph node, adrenal gland, pituitary gland, retina, and autonomic ganglia were examined by light and electron microscopy. Prominent lipidosis-like alterations were seen in all tissues inspected. The results support a previously proposed concept that there is a relationship between the amphiphilic cationic character of a compound and its ability to cause intralysosomal storage of polar lipids. In addition, tamoxifen caused degeneration and necrosis of adrenocortical cells in the zona fasciculata and zona reticularis; this finding is taken as a specific effect of tamoxifen, probably due to its endocrine activity rather than being related to its lipidosis-inducing potency.
Url:
DOI: 10.1016/0041-008X(81)90014-4
Affiliations:
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Le document en format XML
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<term>Generalized lipidosis</term>
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<term>Lamellar inclusions</term>
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<term>Nucleus supraopticus</term>
<term>Polar lipids</term>
<term>Present findings</term>
<term>Rat</term>
<term>Rats subchronically</term>
<term>Reticularis</term>
<term>Retinal pigment epithelium</term>
<term>Side chain</term>
<term>Soleus muscle</term>
<term>Tamoxifen</term>
<term>Tamoxifen citrate</term>
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<front><div type="abstract" xml:lang="en">Abstract: The antiestrogenic drug tamoxifen is an amphiphilic cationic compound and might therefore be suspected to interfere with intralysosomal catabolism of polar lipids as previously observed with several other amphiphilic cationic drugs. Large oral doses (100–130 mg/kg) of tamoxifen were administered to rats for 6 to 14 weeks. Tissues including liver, lung, lymph node, adrenal gland, pituitary gland, retina, and autonomic ganglia were examined by light and electron microscopy. Prominent lipidosis-like alterations were seen in all tissues inspected. The results support a previously proposed concept that there is a relationship between the amphiphilic cationic character of a compound and its ability to cause intralysosomal storage of polar lipids. In addition, tamoxifen caused degeneration and necrosis of adrenocortical cells in the zona fasciculata and zona reticularis; this finding is taken as a specific effect of tamoxifen, probably due to its endocrine activity rather than being related to its lipidosis-inducing potency.</div>
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