TCDD Dotaz Zobrazit nápovědu
Humic substances (HS) are ubiquitous natural products of decomposition of dead organic matter. HS is present in most freshwaters at concentrations ranging from 0.5 to 50mg L(-1). Organic carbon can represent 20% dry weight of sediments. Recently, the interaction of dissolved HS with the aryl hydrocarbon receptor (AhR) has been demonstrated. The AhR is a cytosolic receptor to which persistent organic pollutants (POPs) can bind and many of their toxic effects are mediated through interactions with this receptor. We describe in vitro effects (using H4IIE-luc cells) of binary mixtures of various HS with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), since in contaminated environments these compounds occur simultaneously. Six out of 12 HS samples activated AhR even at environmentally relevant concentrations (17 mg L(-1)), but did not reach the full AhR-activation even at excessive concentration. In simultaneous exposure of H4IIE-luc to HS (17 mg L(-1)) and TCDD (1.2 pM) without any preincubation prior to exposure, either significant additive or facilitative effects were observed. No negative interactions, due to possible sorption of TCDD to HS was observed. Nevertheless, if the HS-TCDD binary mixture was preincubated for 6 days prior to the exposure on H4IIE-luc cells, the additive and facilitative effects were less due to possible sorption of TCDD onto HS. Similar results were obtained from analogous experiments with greater concentrations of both TCDD and HS.
- MeSH
- huminové látky toxicita MeSH
- kinetika MeSH
- krysa rodu rattus MeSH
- látky znečišťující půdu toxicita MeSH
- nádorové buněčné linie MeSH
- polychlorované dibenzodioxiny toxicita MeSH
- receptory aromatických uhlovodíků metabolismus MeSH
- regenerace a remediace životního prostředí metody MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
Past reports have correlated a diagnosis of porphyria cutanea tarda (PCT) with exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Re-examination of the literature, however, has caused us to question the conclusion of a relationship between acquired PCT and TCDD. The major considerations at issue were: (1) whether the diagnostic label of PCT was applied excessively to cases with findings that are nonspecific; (2) whether the clinical conditions suggestive of PCT were the likely results of exposure to another chemical, for example hexachlorobenzene (HCB); and (3) whether a causal link between PCT and TCDD is reasonably substantiated by the facts. Based on the re-evaluation of the literature, the known effects of HCB and TCDD, and the follow-up results from the chemical plant, we submit that HCB alone, or HCB in combination with other polychlorinated aromatic hydrocarbons, may have been responsible for the effects observed and the subsequent correlation to PCT.
- MeSH
- dioxiny otrava MeSH
- dospělí MeSH
- kožní nemoci chemicky indukované epidemiologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- nemoci z povolání chemicky indukované epidemiologie MeSH
- polychlorované dibenzodioxiny otrava MeSH
- porfyrie chemicky indukované epidemiologie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- kazuistiky MeSH
- přehledy MeSH
- Geografické názvy
- Československo MeSH
- New Jersey MeSH
The environmental contaminant 2,3,7,8-tetrachlordibenzo-p-dioxin (TCDD) belongs to the category of highly toxic, persistent organic pollutants that accumulate in animal fat and plant tissues. Today, background TCDD levels in human fat are showing a decreasing trend. The food chain is the main source of exposure in the human population. TCDD regulates the expression of a wide range of drug-metabolizing enzymes and has an impact on a large number of biological systems. The most pronounced effects have occurred in occupational settings following the uncontrolled formation of TCDD after industrial accidents, as well as in rare intentional intoxications. Although the acute effects of TCDD exposure are well described in the literature, the long-term consequences have been underevaluated. The most well-known symptoms of severe acute intoxication are chloracne, porphyria, transient hepatotoxicity, and peripheral and central neurotoxicity. Because of the long-term persistence of TCDD in the human body, atherosclerosis, hypertension, diabetes, vascular ocular changes, and signs of neural system damage, including neuropsychological impairment, can be present several decades after massive exposure. Such chronic effects are nonspecific, multifactorial, and may be causally linked to TCDD only in heavily intoxicated subjects. This opinion is supported by the dose-dependent effect of TCDD found in exposed workers and by experimental animal studies.
- MeSH
- ateroskleróza chemicky indukované MeSH
- diabetes mellitus chemicky indukované MeSH
- financování organizované MeSH
- hypertenze chemicky indukované MeSH
- látky znečišťující životní prostředí toxicita MeSH
- lidé MeSH
- nemoci nervového systému chemicky indukované MeSH
- oční nemoci chemicky indukované MeSH
- polychlorované dibenzodioxiny toxicita MeSH
- vystavení vlivu životního prostředí škodlivé účinky MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- přehledy MeSH
We used 2,3,8,9-tetrachlorodibenzo-p-dioxin (TCDD) and dexamethasone (DEX) to examine their effects on aryl hydrocarbon receptor (AhR) and glucocorticoid receptor (GR) in HeLa cells. TCDD (5 nM), DEX (100 nM) and their combination down-regulated GR after 24 h. DEX reversed AhR mRNA increase and AhR protein decrease caused by TCDD. Since AhR-GR cross-talk occurs in cell-type and species-specific manner, the presented data may serve as the basis in the understanding of mechanisms underlying mutual interactions between AhR and GR.
- MeSH
- dexamethason farmakologie MeSH
- down regulace účinky léků MeSH
- financování organizované MeSH
- glukokortikoidy farmakologie MeSH
- HeLa buňky MeSH
- látky znečišťující životní prostředí toxicita MeSH
- lidé MeSH
- messenger RNA metabolismus účinky léků MeSH
- nádory děložního čípku metabolismus MeSH
- polychlorované dibenzodioxiny toxicita MeSH
- receptory aromatických uhlovodíků metabolismus účinky léků MeSH
- receptory glukokortikoidů metabolismus účinky léků MeSH
- Check Tag
- lidé MeSH
- ženské pohlaví MeSH
Vascular function was examined in subjects with long-term high level of serum 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) during their follow-up visits. Their earlier mean peak TCDD level at the time of exposure in 1965-1968 was estimated in the range of 3300-74 000 pg/g lipids. Ten former pesticide production workers heavily exposed to TCDD (age 57 +/- 2 years, TCDD about 170 pg/g lipids) were examined in 2001. Extended group of 15 TCDD-exposed men (age 59 +/- 3 years, TCDD about 130 pg/g lipids) underwent the same examination in 2004. Findings were compared with a control group of 14 healthy men (age 54 +/- 2 years). Skin microvascular reactivity (MVR) was measured by laser Doppler perfusion monitoring in the forearm during post-occlusive reactive hyperemia (PORH) and thermal hyperemia (TH). Several parameters of MVR in men exposed to TCDD were significantly impaired, compared with the control group and further progression of the impairment of MVR has been observed between years 2001 and 2004. Serum concentration of E-selectin and inhibitor of tissue plasminogen activator 1 (PAI-1) was significantly higher in exposed subjects (56.0 +/- 18.4 ng/mL versus 40.0 +/- 12.0 ng/mL, P = 0.022 and 90.9 +/- 33.3 ng/mL versus 45.0 +/- 18.0, P = 0.002, respectively). In addition, PORH in the forearm was significantly negatively associated with SOD activity (r = -0.77, P = 0.009) as well as the velocity of perfusion increase during TH (r = -0.68, P = 0.03) and TH% (r = -0.78, P = 0.008). Our data document the presence of endothelial dysfunction in TCDD-exposed men.
- MeSH
- časové faktory MeSH
- cévní endotel patofyziologie účinky léků MeSH
- financování organizované MeSH
- hyperemie patofyziologie MeSH
- inhibitor aktivátoru plazminogenu 1 krev MeSH
- kardiovaskulární nemoci chemicky indukované krev patofyziologie MeSH
- kůže krevní zásobení MeSH
- laser doppler flowmetrie MeSH
- lidé MeSH
- lipidy krev MeSH
- mezibuněčná adhezivní molekula-1 krev MeSH
- mikrocirkulace účinky léků MeSH
- následné studie MeSH
- nemoci z povolání chemicky indukované krev chemicky indukované krev patofyziologie MeSH
- pesticidy krev toxicita MeSH
- polychlorované dibenzodioxiny krev toxicita MeSH
- pracovní expozice MeSH
- předloktí krevní zásobení MeSH
- regionální krevní průtok účinky léků MeSH
- rychlost toku krve účinky léků MeSH
- senioři MeSH
- superoxiddismutasa krev MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
