Abstract：
:Hexachlorobenzene (HCB)-induced porphyria occurs in female, but not male, rats after a delay of 35 days following HCB treatment. Uroporphyrinogen decarboxylase (UROD) inhibition has been proposed as a primary causative event. To determine whether there also exists a delay phase and a sexual dimorphism for UROD inhibition, groups of male and female rats were given HCB (100 mg/kg/day) from Days 1 to 5. Hepatic uroporphyrin III was markedly increased only after Day 33. Liver cytosol UROD activity in HCB-treated female rats with porphyria at Days 33, 40, 47, 54, and 100 was decreased by over 70% compared to concurrent control, whereas treated male rats as well as nonporphyric female rats had UROD activity comparable to control levels at Days 6, 12, 19, 26, 33, 40, 47, and 54. Level of immunoreactive UROD in cytosol of porphyric rats was not modified by HCB. No gender-related differences in liver cytosol radiolabel level ([14C]HCB given as the fifth dose) were found at Days 6 and 30. Chromatography of liver cytosol showed nonspecific binding of radiolabel to proteins for males, porphyric and nonporphyric females, and loss of UROD activity did not correlate with the amount of radiolabel in the UROD-containing fractions. Thus, the gender-specific decrease in UROD activity observed when porphyria develops in female rats (delay of about 4 weeks), as well as the persistence of low activity and porphyria for months, suggests that UROD inhibition was causally related to porphyria.
journal_name
Toxicol Appl Pharmacoljournal_title
Toxicology and applied pharmacologyauthors
Mylchreest E,Charbonneau Mdoi
10.1006/taap.1997.8157subject
Has Abstractpub_date
1997-07-01 00:00:00pages
23-33issue
1eissn
0041-008Xissn
1096-0333pii
S0041-008X(97)98157-6journal_volume
145pub_type
杂志文章abstract：:2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a highly toxic environmental pollutant and is well known for inducing thymic atrophy in mice, although the exact mechanism of its action remains unclear. Recent studies from our laboratory demonstrated that TCDD induces apoptosis in thymocytes and that Fas- mice (lpr/lpr) ...
journal_title：Toxicology and applied pharmacology
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doi：10.1006/taap.1998.8390
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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doi：10.1016/j.taap.2008.09.024
更新日期：2009-01-01 00:00:00
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journal_title：Toxicology and applied pharmacology
pub_type： 杂志文章
doi：10.1006/taap.1999.8709
更新日期：1999-08-01 00:00:00
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journal_title：Toxicology and applied pharmacology
pub_type： 杂志文章
doi：10.1006/taap.1995.1101
更新日期：1995-06-01 00:00:00
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journal_title：Toxicology and applied pharmacology
pub_type： 杂志文章
doi：10.1006/taap.1994.1087
更新日期：1994-05-01 00:00:00
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journal_title：Toxicology and applied pharmacology
pub_type： 杂志文章
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更新日期：1991-03-15 00:00:00
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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doi：10.1006/taap.1996.0301
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abstract：:Brominated flame retardants (BFRs) are present in many consumer products ranging from fabrics to plastics and electronics. Wide use of flame retardants can pose an environmental hazard and it is of interest to determine the mechanism of their toxicity. Of all the BFRs, 3,3',5,5'-tetrabromobisphenol A (TBBPA) is produc...
journal_title：Toxicology and applied pharmacology
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更新日期：2008-07-01 00:00:00
abstract：:Guttiferone-A (GA) is a natural occurring polyisoprenylated benzophenone with cytotoxic action in vitro and anti-tumor action in rodent models. We addressed a potential involvement of mitochondria in GA toxicity (1-25 μM) toward cancer cells by employing both hepatic carcinoma (HepG2) cells and succinate-energized mit...
journal_title：Toxicology and applied pharmacology
pub_type： 杂志文章
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更新日期：2011-06-15 00:00:00
