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dc.contributor.authorKlimczak, Michal
dc.contributor.authorDarago, Adam
dc.contributor.authorBruchajzer, Elzbieta
dc.contributor.authorDomeradzka-Gajda, Katarzyna
dc.contributor.authorStępnik, Maciej
dc.contributor.authorKuzajska, Katarzyna
dc.contributor.authorKilanowicz, Anna
dc.date.accessioned2018-06-04T09:46:00Z
dc.date.available2018-06-04T09:46:00Z
dc.date.issued2018-06
dc.identifier.citationEnviron. Toxicol. 2018, 33 (6):695-705en
dc.identifier.issn1522-7278
dc.identifier.pmid29663608
dc.identifier.doi10.1002/tox.22558
dc.identifier.urihttp://hdl.handle.net/10146/618210
dc.description.abstractHexachloronaphthalenes (HxCNs) are the most toxic congeners of polychlorinated naphthalenes, a group of compounds lately included into the list of persistent organic pollutants (POPs). This study presents the effects of 90-day intragastric administration of HxCN to female Wistar rats at doses of 0.03, 0.1, and 0.3 mg/kg body weight. The study examined selected parameters of the heme synthesis pathway, oxidative stress, hepatic cytochromes level, and basic hematology indicators. A micronucleus test was also performed. The subchronic exposure of rats to HxCN resulted in disruption of heme biosynthesis, hematological disturbances, and hepatotoxicity. The highest dose of HxCN inhibited aminolevulinic acid dehydratase (ALA-D) and uroporphyrinogen decarboxylase (URO-D). Accumulation of higher carboxylated porphyrins in the liver and increased excretion of 5-aminolevulinic acid in the urine was observed after a dose of 0.1 mg/kg body weight. The most sensitive effect of HxCN in rats was very strong induction of hepatic CYP1A1 activity, which was observed after the lowest dose. The highest dose of HxCN induced significant thrombocytopenia, thymic atrophy and hepatotoxicity, expressed as hepatomegaly and hepatic steatosis.
dc.description.sponsorshipMedical University of Lodz, Poland, Grant Numbers: 503/3-045-01/503-31-001, 502-03/3-045-01/502-34-044en
dc.language.isoenen
dc.relation.urlhttps://onlinelibrary.wiley.com/doi/epdf/10.1002/tox.22558en
dc.rightsArchived with thanks to Environmental toxicologyen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectCYP1A1en
dc.subjectheme biosynthesisen
dc.subjecthexachloronaphthaleneen
dc.subjectraten
dc.subjecttoxicityen
dc.titleThe effects of hexachloronaphthalene on selected parameters of heme biosynthesis and systemic toxicity in female wistar rats after 90-day oral exposure.en
dc.typeArticleen
dc.contributor.departmentNofer Institute of Occupational Medicine, Lodz, Polanden
dc.identifier.journalEnvironmental toxicologyen
refterms.dateFOA2018-12-17T18:09:55Z
html.description.abstractHexachloronaphthalenes (HxCNs) are the most toxic congeners of polychlorinated naphthalenes, a group of compounds lately included into the list of persistent organic pollutants (POPs). This study presents the effects of 90-day intragastric administration of HxCN to female Wistar rats at doses of 0.03, 0.1, and 0.3 mg/kg body weight. The study examined selected parameters of the heme synthesis pathway, oxidative stress, hepatic cytochromes level, and basic hematology indicators. A micronucleus test was also performed. The subchronic exposure of rats to HxCN resulted in disruption of heme biosynthesis, hematological disturbances, and hepatotoxicity. The highest dose of HxCN inhibited aminolevulinic acid dehydratase (ALA-D) and uroporphyrinogen decarboxylase (URO-D). Accumulation of higher carboxylated porphyrins in the liver and increased excretion of 5-aminolevulinic acid in the urine was observed after a dose of 0.1 mg/kg body weight. The most sensitive effect of HxCN in rats was very strong induction of hepatic CYP1A1 activity, which was observed after the lowest dose. The highest dose of HxCN induced significant thrombocytopenia, thymic atrophy and hepatotoxicity, expressed as hepatomegaly and hepatic steatosis.


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Archived with thanks to Environmental toxicology
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