| Testosterone metabolites in patients reduce the levels of very long chain fatty acids accumulated in X-adrenoleukodystrophic fibroblasts. | |
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MedLine Citation:
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PMID: 10904139 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Testosterone metabolites (dihydrotestosterone, DHT) and 5 alpha-androstan-3 alpha,17 beta-diol (3 alpha-diol), but not testosterone itself, were shown to reduce the levels of very long chain fatty acids which accumulate in cultured skin fibroblasts from X-adrenoleukodystrophic patients (X-ALD). In addition, in X-ALD fibroblasts, testosterone is less actively converted into DHT vs. controls (skin fibroblasts retrieved from normal subjects) whereas the additional conversion of DHT to the final product 3 alpha-diol is enhanced. This is the first report of altered testosterone metabolism in X-ALD fibroblasts and of the effects of androgens in lowering the abnormal accumulation of very long chain fatty acids in this type of cells. |
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Authors:
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A Petroni; N Papini; M Blasevich; V Magnaghi; I Cavarretta; C Galli; R C Melcangi |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Neuroscience letters Volume: 289 ISSN: 0304-3940 ISO Abbreviation: Neurosci. Lett. Publication Date: 2000 Aug |
Date Detail:
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Created Date: 2000-10-02 Completed Date: 2000-10-02 Revised Date: 2004-11-17 |
Medline Journal Info:
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Nlm Unique ID: 7600130 Medline TA: Neurosci Lett Country: IRELAND |
Other Details:
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Languages: eng Pagination: 139-42 Citation Subset: IM |
Affiliation:
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Institute of Pharmacological Sciences, University of Milan, via Balzaretti 9, 20133, Milan, Italy. anna.petroni@unimi.it |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adrenoleukodystrophy
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metabolism*,
pathology Child Dihydrotestosterone / metabolism Fatty Acids / metabolism* Fibroblasts / metabolism* Humans Skin / cytology, metabolism, pathology Testosterone / metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Fatty Acids; 506-46-7/hexacosanoic acid; 521-18-6/Dihydrotestosterone; 557-59-5/lignoceric acid; 58-22-0/Testosterone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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