| The decrease in uroporphyrinogen decarboxylase activity induced by ethanol predisposes rats to the development of porphyria and accelerates xenobiotic-triggered porphyria, regardless of hepatic damage. | |
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MedLine Citation:
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PMID: 12426626 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We evaluated the porphyrinogenic ability of ethanol (20% in drinking water) per se, its effect on the development of sporadic porphyria cutanea tarda induced by hexachlorobenzene in female Wistar rats (170-190 g, N = 8/group), and the relationship with hepatic damage. Twenty-five percent of the animals receiving ethanol increased up to 14-, 25-, and 4.5-fold the urinary excretion of delta-aminolevulinate, porphobilinogen, and porphyrins, respectively. Ethanol exacerbated the precursor excretions elicited by hexachlorobenzene. Hepatic porphyrin levels increased by hexachlorobenzene treatment, while this parameter only increased (up to 90-fold) in some of the animals that received ethanol alone. Ethanol reduced the activities of uroporphyrinogen decarboxylase, delta-aminolevulinate dehydrase and ferrochelatase. In the ethanol group, many of the animals showed a 30% decrease in uroporphyrinogen activity; in the ethanol + hexachlorobenzene group, this decrease occurred before the one caused by hexachlorobenzene alone. Ethanol exacerbated the effects of hexachlorobenzene, among others, on the rate-limiting enzyme delta-aminolevulinate synthetase. The plasma activities of enzymes that are markers of hepatic damage were similar in all drug-treated groups. These results indicate that 1) ethanol exacerbates the biochemical manifestation of sporadic hexachlorobenzene-induced porphyria cutanea tarda; 2) ethanol per se affects several enzymatic and excretion parameters of the heme metabolic pathway; 3) since not all the animals were affected to the same extent, ethanol seems to be a porphyrinogenic agent only when there is a predisposition, and 4) hepatic damage showed no correlation with the development of porphyria cutanea tarda. |
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Authors:
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M C Ríos de Molina; M B Mazzetti; M Galigniana; C Aldonatti; J M Tomio; L C San Martín de Viale |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Brazilian journal of medical and biological research = Revista brasileira de pesquisas médicas e biológicas / Sociedade Brasileira de Biofísica ... [et al.] Volume: 35 ISSN: 0100-879X ISO Abbreviation: Braz. J. Med. Biol. Res. Publication Date: 2002 Nov |
Date Detail:
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Created Date: 2002-11-11 Completed Date: 2003-04-02 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8112917 Medline TA: Braz J Med Biol Res Country: Brazil |
Other Details:
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Languages: eng Pagination: 1273-83 Citation Subset: IM |
Affiliation:
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Laboratorio de Porfirias Experimentales y Metabolismo del Hemo, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cytochrome P-450 Enzyme System / analysis Disease Models, Animal Ethanol / pharmacology* Female Ferrochelatase / drug effects*, metabolism Hexachlorobenzene Liver / drug effects*, enzymology, pathology Porphobilinogen / urine Porphobilinogen Synthase / urine Porphyria Cutanea Tarda / chemically induced*, enzymology, urine Porphyrins / urine Rats Rats, Wistar Solvents / pharmacology* Uroporphyrinogen Decarboxylase / drug effects*, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Porphyrins; 0/Solvents; 118-74-1/Hexachlorobenzene; 487-90-1/Porphobilinogen; 64-17-5/Ethanol; 9035-51-2/Cytochrome P-450 Enzyme System; EC 4.1.1.37/Uroporphyrinogen Decarboxylase; EC 4.2.1.24/Porphobilinogen Synthase; EC 4.99.1.1/Ferrochelatase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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