کد مقاله کد نشریه سال انتشار مقاله انگلیسی ترجمه فارسی نسخه تمام متن
2517089 1118923 2019 4 صفحه PDF سفارش دهید دانلود کنید
عنوان انگلیسی مقاله
Uroporphyria produced in mice by iron and 5-aminolevulinic acid
موضوعات مرتبط
علوم پزشکی و سلامت داروسازی، سم شناسی و علوم دارویی داروشناسی
پیش نمایش صفحه اول مقاله
Uroporphyria produced in mice by iron and 5-aminolevulinic acid
چکیده انگلیسی
Porphyria cutanea tarda and the analogous hepatic uroporphyria produced in rodents by aromatic hydrocarbons result from inactivation of hepatic uroporphyrinogen decarboxylase (UROD). Inactivation appears to be iron-dependent and may require induction of cytochromes of the P450IA subfamily. To investigate the hypothesis that the mechanism of inactivation involves an intermediate of haem biosynthesis, we administered iron and the haem precursor, 5-aminolevulinate (ALA), to mice. Iron-overloaded male mice of the Ah-responsive C57BL/6 strain, given ALA solution as their only drink, developed severe uroporphyria after 49 days. ALA did not produce uroporphyria in ironoverloaded male mice of the Ah-nonresponsive DBA/2 strain. Iron or ALA alone did not produce porphyria in either strain. Hepatic iron concentrations and rates of ethoxyresorufin deethylation (an indicator of cytochrome P450IA-mediated activity) were similar in both strains. These experiments show that a haem precursor is involved in iron-dependent inactivation of UROD. They emphasize the importance of inherited factors in determining susceptibility to this type of porphyria, even in the absence of administration of compounds that act through the Ah locus to induce cytochromes of the P450IA subfamily.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical Pharmacology - Volume 41, Issue 12, 15 June 1991, Pages 2019-2022
نویسندگان
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