Диоксины

вопросы современной биологической химии, молекулярной биологии, химической энзимологии и смежных наук
biochem, molbio, chemical enzymology and related discussions for professionals
Ответить
Mary-shka
Сообщения: 20
Зарегистрирован: Ср мар 12, 2008 10:02 am

Диоксины

Сообщение Mary-shka » Чт мар 20, 2008 8:49 am

Есть ли информаци о микороорганизмах или вообще организмах стойких к действию диоксинов?

Аватара пользователя
ИСН
Робин Гуд
Сообщения: 8532
Зарегистрирован: Пт окт 10, 2003 5:32 pm
Контактная информация:

Сообщение ИСН » Чт мар 20, 2008 10:01 am

(В сторону) Один такой организм руководит соседней страной.

Аватара пользователя
avor
Сообщения: 12650
Зарегистрирован: Пн янв 24, 2005 1:13 pm

Re: Диоксины

Сообщение avor » Чт мар 20, 2008 6:43 pm

Mary-shka писал(а):Есть ли информаци о микороорганизмах или вообще организмах стойких к действию диоксинов?
На запрос: "organism dioxin resistance TCDD"

pubmed
отвечает двумя ссылками.

[Immunotoxicology in occupational and environmental medicine: prospectives,
limitations, and research objectives]

[Article in Italian]

Colosio C, Barcellini W, Corsini E.

International Centre for Pesticide Safety, Busto Garolfo, MI.

The immune system is able to recognize and neutralize potentially harmful agents,
conferring to the organism resistance to infectious and malignant diseases. The
authors have reviewed the literature and identified a group of substances able to
enhance and/or reduce different immune functions, both in an experimental model
and in occupational and environmental human exposure. The group includes several
polyhalogenated hydrocarbons, particularly polychlorinated biphenyls,
polybrominated biphenyls, tetrachloro-dibenzo-p-dioxin (TCDD), some metals like
lead, cadmium and mercury, pesticides, i.e. dithiocarbamates and organotin
compounds, organic solvents. The observed changes are usually slight and do not
allow prognostic conclusion. In this study, the authors propose a 3-level rank of
tests suitable for the immune evaluation of individuals occupationally exposed to
xenobiotics, divided into three levels, as follows: tier 1: immunoglobulin
classes (IgG, IgA, IgM), complement fractions (C3, C4), rheumatoid factor, and
non-organ specific autoantibodies (AMA, SMA, ANA); CD3, CD4, CD8, CD57, CD20,
HLA-DR; CD3/HLA-DR positive lymphocyte subsets; tier 2: determination of the
mitotic response of peripheral blood lymphocytes to phytohaemoagglutinin,
anti-CD3 monoclonal antibody, phorbol-myristate-acetate (PMA) and polyclonal
immunoglobulin production after stimulation with pokeweed mitogen; tier 3:
cytokine production with and without mitogen stimulation. The approach is "step
by step" and assumes the need of a closely integrated and comparative evaluation
of the findings obtained. The protocol could be used in research fields;
moreover, some of the tests could be useful in the monitoring of persons exposed
in the environment or in the workplace to immunotoxic substances or to biological
agents.

Publication Types:
English Abstract
Review

PMID: 9734191 [PubMed - indexed for MEDLINE]

2: J Submicrosc Cytol Pathol. 1998 Jan;30(1):157-63.

Interaction of PCB congeners and 2,3,7,8-TCDD in the rat liver: an electron
microscope study.

Connell BJ, Singh A, Chu I.

Atlantic Veterinary College, University of Prince Edward Island, Charlottetown,
Canada.

Polyhalogenated aromatic compounds such as polychlorinated biphenyls (PCBs) and
polychlorinated dibenzo-p-dioxins continue to be environmental contaminants
because of their bioaccumulation in the food chain and resistance to
biodegradation. This study was undertaken to determine if WHO-IPCS PCB congeners
or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) individually or their
coadministration in rats produced morphological alterations in the liver. Groups
(N = 5) of female Sprague Dawley rats received TCDD (0, 2.5, 25, 250, 1,000 ng/kg
bw/day) or PCB (0, 2, 20 micrograms/kg bw/day) either alone, or each dose of PCB
coadministered with that of TCDD. The test substances were dissolved in corn oil
and given by gavage at 0.2 ml/100 g bw/day for 28 days. At the end of the
experiment the rats were killed and liver samples were prepared for transmission
electron microscopy. Electron micrographs of the liver from animals of the
control groups revealed characteristic normal hepatocyte architecture. An
increase in smooth endoplasmic reticulum (SER) profiles and a corresponding
decrease in the profiles of rough endoplasmic reticulum (RER) proportional to the
increased doses of the compounds was revealed in the micrographs.
Coadministration of PCBs and TCDD induced greater SER proliferation and a greater
decrease in the number of RER profiles compared to either compound administered
individually. The PCBs and TCDD at the doses used apparently interacted to induce
hepatic ultrastructural alterations. These changes may represent an attempt by
the organism to metabolize and neutralize the effects of xenobiotics.

PMID: 9530863 [PubMed - indexed for MEDLINE]

В общем медицине и биологии, на сегодня, такие органоны не известны. :(

Polychemist
Сообщения: 9647
Зарегистрирован: Вт дек 21, 2004 11:42 am

Сообщение Polychemist » Пт мар 21, 2008 5:05 am

Вопрос был не по животным, а вообще о живых организмах. Вот тут я не понял последней фразы о natural killers.

Author(s): Zabrodskiy, P. F.; Troshkin, N. M.; Merkina, C. M.; Mandych, V. G.
Source: Toksikologicheskii Vestnik Issue: 6 Pages: 14-17 Published: November 2004
Abstract: It was established in experiments on non-inbred rats that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) at single doses of 1-8 mug/kg causes a dose-dependent reduction of main parameters of non-specific resistance in the organism, reduced formation of antibodies mainly to T-independent antigen and of type-delayed hypersensitivity response. TCDD in doses used did not practically influence the activity of natural killers.

Polychemist
Сообщения: 9647
Зарегистрирован: Вт дек 21, 2004 11:42 am

Сообщение Polychemist » Пт мар 21, 2008 5:40 am

Ближе к делу:
Author(s): Hahn ME, Karchner SI, Franks DG, Merson RR
Aryl hydrocarbon receptor polymorphisms and dioxin resistance in Atlantic killifish (Fundulus heteroclitus)
Source: PHARMACOGENETICS Volume: 14 Issue: 2 Pages: 131-143 Published: FEB 2004
Times Cited: 9 References: 97
Abstract: The aryl hydrocarbon receptor (AHR) gene encodes a ligand-activated transcription factor through which planar halogenated aromatic hydrocarbons (HAHs) such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as well as polynuclear aromatic hydrocarbons (PAHs) cause altered gene expression and toxicity. To understand the role of AHR genetic variability in differential sensitivity to HAHs and PAHs, we are currently studying a population of the teleost Fundulus heteroclitus (Atlantic killifish) that has evolved genetic resistance to the toxic and biochemical effects of these compounds. Here, we report that the killifish AHR1 locus is highly polymorphic and that the frequencies of the major allele types differ between dioxinsensitive and dioxin-resistant populations. Twenty-five single nucleotide polymorphisms (SNPs), nine of which are non-synonymous, were identified in the AHR1 coding sequence. Seven identified alleles were assigned to three groups, designated AHR1*1, AHR1*2 and AHR1*3. AHR1*1 alleles were under-represented in a population of dioxin- and polychlorinated biphenyl (PCB)-resistant fish from a PCB-contaminated Superfund site (New Bedford Harbor, Massachusetts, USA) compared to dioxin-sensitive fish from a less contaminated reference site (Scorton Creek, Massachusetts, USA). To determine the possible role of these AHR1 variants in differential HAH sensitivity, we expressed representative variant proteins from the two most divergent allelic groups (AHR1*1 and AHR1*3) by in-vitro transcription and translation and assessed their functional properties. AHR1*1A and AHR1*3A proteins displayed similar binding capacities and affinities for [H-3]TCDD. In transient transfection assays using mammalian cells, AHR1*1A and AHR1*3A exhibited similar abilities to support TCDD-dependent transactivation of a luciferase reporter gene under control of AHR-responsive enhancer elements. We discuss the possibility of other functional differences in AHR1 variants or their interaction with other killifish loci (AHR2, AHRR) that may contribute to differences in dioxin sensitivity.

Polychemist
Сообщения: 9647
Зарегистрирован: Вт дек 21, 2004 11:42 am

Сообщение Polychemist » Пт мар 21, 2008 5:47 am

Кинул в обменник результаты поиска по "dioxin resistance" в ISI

Ответить

Вернуться в «биохимия и молекулярная биология / biochemistry and molecular biology»

Кто сейчас на конференции

Сейчас этот форум просматривают: нет зарегистрированных пользователей и 5 гостей