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#11
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Exposure to Chemical Pollutants Increases Fat
citation for the above?
Dioxin: a review of its environmental effects and its aryl hydrocarbon receptor biology. A highly persistent trace environmental contaminant and one of the most potent toxicants known is dioxin (2,3,7,8-tetrachlorodibenzo-para- dioxin or TCDD). TCDD induces a broad spectrum of biological responses, including induction of cytochrome P-450 1A1 (CYP1A1), disruption of normal hormone signaling pathways, reproductive and developmental defects, immunotoxicity, liver damage, wasting syndrome, and cancer. Its classification was upgraded from "possible human carcinogen" (group 2B) to "human carcinogen" (group 1) by the International Agency for Research on Cancer (IARC) in 1997. Exposure to TCDD may also cause changes in sex ratio, and tumor promotion in other animals. Because of the growing public and scientific concern, toxicological studies have been initiated to analyze the short- and long-term effects of dioxin. TCDD brings about a wide variety of toxic and biochemical effects via aryl hydrocarbon receptor (AhR)-mediated signaling pathways. Essential steps in this adaptive mechanism include AhR binding of ligand in the cytoplasm of cells associated with two molecules of chaperone heatshock protein (Hsp90) and AhR interactive protein, translocation of the receptor to the nucleus, dimerization with the Ah receptor nuclear translocator, and binding of this heterodimeric transcription factor (present in CYP1A) to dioxin- responsive elements upstream of promoters that regulate the expression of genes involved in xenobiotic metabolism. PMID: 15900503 |
#12
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Exposure to Chemical Pollutants Increases Fat
Do you have a citation for the above?
2,3,7,8-Tetrachlorodibenzo-p-dioxin induces apoptotic cell death and cytochrome P4501A expression in developing Fundulus heteroclitus embryos. Fundulus heteroclitus embryos were exposed to 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD) during early development using nanoinjection or water bath exposure. TCDD caused developmental abnormalities that included hemorrhaging, loss of vascular integrity, edema, stunted development and death. The LC(50) and LD(50) of TCDD for Fundulus embryos were approximately 19.7+/-9.5 pg TCDD/microl (water bath) and 0.25+/-0.09 ng TCDD/g embryo (nanoinjection). To identify a possible cause for these developmental abnormalities we analyzed the effects of TCDD on apoptotic cell death and cytochrome P4501A (CYP1A) expression in the embryos. TCDD exposure increased apoptotic cell death in several tissues including brain, eye, gill, kidney, tail, intestine, heart, and vascular tissue. CYP1A expression was also increased in the TCDD-exposed embryos predominantly in liver, kidney, gill, heart, intestine, and in vascular tissues throughout the embryo. There was co-occurrence of TCDD-induced apoptosis and CYP1A expression in some, but not all, cell types. In addition the dose response relationships for apoptosis and mortality were similar, while CYP1A expression appeared more sensitive to TCDD induction. PMID: 11311389 |
#13
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Exposure to Chemical Pollutants Increases Fat
... citation for the above?
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) alters the mRNA expression of critical genes associated with cholesterol metabolism, bile acid biosynthesis, and bile transport in rat liver: a microarray study. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent hepatotoxin that exerts its toxicity through binding to the aryl hydrocarbon receptor (AhR) and the subsequent induction or repression of gene transcription. In order to further identify novel genes and pathways that may be associated with TCDD-induced hepatotoxicity, we investigated gene changes in rat liver following exposure to single oral doses of TCDD. Male Sprague-Dawley rats were administered single doses of 0.4 microg/kg bw or 40 microg/kg bw TCDD and killed at 6 h, 24 h, or 7 days, for global analyses of gene expression. In general, low-dose TCDD exposure resulted in greater than 2-fold induction of genes coding for a battery of phase I and phase II metabolizing enzymes including CYP1A1, CYP1A2, NADPH quinone oxidoreductase, UGT1A6/7, and metallothionein 1. However, 0.4 microg/kg bw TCDD also altered the expression of Gadd45a and Cyclin D1, suggesting that even low-dose TCDD exposure can alter the expression of genes indicative of cellular stress or DNA damage and associated with cell cycle control. At the high-dose, widespread changes were observed for genes encoding cellular signaling proteins, cellular adhesion, cytoskeletal and membrane transport proteins as well as transcripts coding for lipid, carbohydrate and nitrogen metabolism. In addition, decreased expression of cytochrome P450 7A1, short heterodimer partner (SHP; gene designation nr0b2), farnesyl X receptor (FXR), Ntcp, and Slc21a5 (oatp2) were observed and confirmed by RT-PCR analyses in independent rat liver samples. Altered expression of these genes implies major deregulation of cholesterol metabolism and bile acid synthesis and transport. We suggest that these early and novel changes have the potential to contribute significantly to TCDD induced hepatotoxicity and hypercholesterolemia. PMID: 16054898 |
#14
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Exposure to Chemical Pollutants Increases Fat
... citation for the above?
Iron deficiency prevents liver toxicity of 2,3,7,8-tetrachlorodibenzo- p-dioxin. The compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes hepatocellular damage and porphyria in C57B1/6J mice, among a wide range of toxic effects. We compared the effect of TCDD toxicity in iron-deficient mice with that in mice receiving a normal diet. Porphyria did not develop in the iron-deficient animals, and these animals were also protected from hepatocellular damage and certain other toxic effects of TCDD. PMID: 432648 |
#15
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Exposure to Chemical Pollutants Increases Fat
Some POPs alter cells via a non-ROS mechanisms ...
Do you have a citation for the above? 2,3,7,8-tetrachlorobenzo-p-dioxin inhibits proliferation of SK-N-SH human neuronal cells through decreased production of reactive oxygen species. Oxidative stress has been known to be involved in the mechanism of toxic effects of various agents on many cellular systems. In this study we investigated the role of reactive oxygen species (ROS) in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced neuronal cell toxicity using SK-N-SH human neuroblastoma cells. TCDD inhibited proliferation of the cells in a dose-dependent manner, which was revealed by MTT staining, counting of cells stained with trypan blue and [3H]thymidine uptake assay. TCDD also suppressed the basal generation of ROS in a time- and concentration-dependent manner assessed by 2',7'-dichlorofluorescein fluorescence. In addition, TCDD induced a dose-dependent inhibition of lipid peroxidation, a biomarker of oxidative stress, whereas it significantly increased the level of glutathione (GSH), an intracellular free radical scavenger in the cells. Moreover, TCDD altered the activities of major antioxidant enzymes; increase in superoxide dismutase (SOD) and catalase, but decrease in glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Red). Pretreatment with L-buthionine-S,R-sulfoximine (BSO, 50 microM), an inhibitor of GSH synthesis, significantly prevented the TCDD-induced reduction in lipid peroxidation and cell proliferation. Interestingly, exogenous application of an oxidant, H2O2 (50 microM) markedly restored the inhibited cell proliferation induced by TCDD. Taken together, these results suggest that alteration of cellular redox balance may mediate the TCDD-induced inhibition of proliferation in human neuronal cells. PMID: 12607819 |
#16
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Exposure to Chemical Pollutants Increases Fat
citation for the above?
Neural precursor cell proliferation is disrupted through activation of the aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Neurogenesis involves the proliferation of multipotent neuroepithelial stem cells followed by differentiation into lineage-restricted neural precursor cells (NPCs) during the embryonic period. Interestingly, these progenitor cells express robust levels of the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that regulates expression of genes important for growth regulation, and xenobiotic metabolism. Upon binding 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a pervasive environmental contaminant and potent AhR ligand, AhR, is activated and disrupts gene expression patterns to produce cellular toxicity. Because of its widespread distribution in the brain during critical proliferative phases of neurogenesis, it is conceivable that AhR participates in NPC expansion. Therefore, this study tested the hypothesis that AhR activation by TCDD disrupts signaling events that regulate NPC proliferation. The C17.2 NPC line served as a model system to (1) assess whether NPCs are targets for TCDD-induced neurotoxicity and (2) characterize the effects of TCDD on NPC proliferation. We demonstrated that C17.2 NPCs express an intact AhR signaling pathway that becomes transcriptionally active after TCDD exposure. (3)H-thymidine and alamar blue reduction assays indicated that TCDD suppresses NPC proliferation in a concentration-dependent manner without the loss of cell viability. Cell cycle distribution analysis by flow cytometry revealed that TCDD-induced growth arrest results from an impaired G1 to S cell cycle transition. Moreover, TCDD exposure altered p27( kip1) and cyclin D1 cell cycle regulatory protein expression levels consistent with a G1 phase arrest. Initial studies in primary NPCs isolated from the ventral forebrain of embryonic mice demonstrated that TCDD reduced cell proliferation through a G1 phase arrest, corroborating our findings in the C17.2 cell line. Together, these observations suggest that the inappropriate or sustained activation of AhR by TCDD during neurogenesis can interfere with signaling pathways that regulate neuroepithelial stem cell/NPC proliferation, which could adversely impact final cell number in the brain and lead to functional impairments. PMID: 20486776 |
#17
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Exposure to Chemical Pollutants Increases Fat
In article
, jay wrote: ... citation for the above? Receptor- and reactive intermediate-mediated mechanisms of teratogenesis. Drugs and environmental chemicals can adversely alter the development of the fetus at critical periods during pregnancy, resulting in death, or in structural and functional birth defects in the surviving offspring. This process of teratogenesis may not be evident until a decade or more after birth. Postnatal functional abnormalities include deficits in brain function, a variety of metabolic diseases, and cancer. Due to the high degree of fetal cellular division and differentiation, and to differences from the adult in many biochemical pathways, the fetus is highly susceptible to teratogens, typically at low exposure levels that do not harm the mother. Insights into the mechanisms of teratogenesis come primarily from animal models and in vitro systems, and involve either receptor-mediated or reactive intermediate-mediated processes. Receptor-mediated mechanisms involving the reversible binding of xenobiotic substrates to a specific receptor are exemplified herein by the interaction of the environmental chemical 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or "dioxin") with the cytosolic aryl hydrocarbon receptor (AHR), which translocates to the nucleus and, in association with other proteins, binds to AH-responsive elements (AHREs) in numerous genes, initiating changes in gene transcription that can perturb development. Alternatively, many xenobiotics are bioactivated by fetal enzymes like the cytochromes P450 (CYPs) and prostaglandin H synthases (PHSs) to highly unstable electrophilic or free radical reactive intermediates. Electrophilic reactive intermediates can covalently (irreversibly) bind to and alter the function of essential cellular macromolecules (proteins, DNA), causing developmental anomalies. Free radical reactive intermediates can enhance the formation of reactive oxygen species (ROS), resulting in oxidative damage to cellular macromolecules and/or altered signal transduction. The teratogenicity of reactive intermediates is determined to a large extent by the balance among embryonic and fetal pathways of xenobiotic bioactivation, detoxification of the xenobiotic reactive intermediate, detoxification of ROS, and repair of oxidative macromolecular damage. PMID: 20020262 Huh? That's all you got? ;O) -- - Billy Mad dog Republicans to the right. Democratic spider webs to the left. True conservatives, and liberals not to be found anywhere in the phantasmagoria of the American political landscape. America is not broke. The country is awash in wealth and cash. It's just that it's not in your hands. It has been transferred, in the greatest heist in history, from the workers and consumers to the banks and the portfolios of the uber-rich. http://www.politifact.com/wisconsin/.../michael-moore /michael-moore-says-400-americans-have-more-wealth-/ |
#18
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Exposure to Chemical Pollutants Increases Fat
In article
, Billy wrote: In article , jay wrote: ... citation for the above? Receptor- and reactive intermediate-mediated mechanisms of teratogenesis. Drugs and environmental chemicals can adversely alter the development of the fetus at critical periods during pregnancy, resulting in death, or in structural and functional birth defects in the surviving offspring. This process of teratogenesis may not be evident until a decade or more after birth. Postnatal functional abnormalities include deficits in brain function, a variety of metabolic diseases, and cancer. Due to the high degree of fetal cellular division and differentiation, and to differences from the adult in many biochemical pathways, the fetus is highly susceptible to teratogens, typically at low exposure levels that do not harm the mother. Insights into the mechanisms of teratogenesis come primarily from animal models and in vitro systems, and involve either receptor-mediated or reactive intermediate-mediated processes. Receptor-mediated mechanisms involving the reversible binding of xenobiotic substrates to a specific receptor are exemplified herein by the interaction of the environmental chemical 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or "dioxin") with the cytosolic aryl hydrocarbon receptor (AHR), which translocates to the nucleus and, in association with other proteins, binds to AH-responsive elements (AHREs) in numerous genes, initiating changes in gene transcription that can perturb development. Alternatively, many xenobiotics are bioactivated by fetal enzymes like the cytochromes P450 (CYPs) and prostaglandin H synthases (PHSs) to highly unstable electrophilic or free radical reactive intermediates. Electrophilic reactive intermediates can covalently (irreversibly) bind to and alter the function of essential cellular macromolecules (proteins, DNA), causing developmental anomalies. Free radical reactive intermediates can enhance the formation of reactive oxygen species (ROS), resulting in oxidative damage to cellular macromolecules and/or altered signal transduction. The teratogenicity of reactive intermediates is determined to a large extent by the balance among embryonic and fetal pathways of xenobiotic bioactivation, detoxification of the xenobiotic reactive intermediate, detoxification of ROS, and repair of oxidative macromolecular damage. PMID: 20020262 Huh? That's all you got? ;O) http://www.scientificamerican.com/article.cfm?id=chemical-controls April 2010, Scientific American p. 30 Chemical Controls Seriously of the more than 80,000 chemicals in use in the U.S., only five have been either restricted or banned. Not 5 percent, five. The EPA has been able to force health and safety testing for only around 200. -- - Billy America is not broke. The country is awash in wealth and cash. It's just that it's not in your hands. It has been transferred, in the greatest heist in history, from the workers and consumers to the banks and the portfolios of the uber-rich. http://www.politifact.com/wisconsin/.../michael-moore /michael-moore-says-400-americans-have-more-wealth-/ You put Lloyd Blankfein in pound-me-in-the-ass prison for one six-month term, and all this bull**** would stop, all over Wall Street. That's all it would take. Just once. |
#19
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Exposure to Chemical Pollutants Increases Fat
Study Finds Exposure to Chemical Pollutants Increases Fat
Rats exposed to high levels of chemical pollutants in fish oil could not regulate fat properly Links to original paper: http://ehp03.niehs.nih.gov/article/f...89/ehp.0901321 or http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854721/ "In this study, we demonstrate for the first time a causal relationship between POPs and insulin resistance in rats. In vivo, chronic exposure to low doses of POPs commonly found in food chains induced severe impairment of whole-body insulin action and contributed to the development of abdominal obesity and hepatosteatosis. Treatment in vitro of differentiated adipocytes with nanomolar concentrations of POP mixtures mimicking those found in crude salmon oil induced a significant inhibition of insulin-dependent glucose uptake. These data provide compelling evidence that exposure to POPs increases the risk of developing insulin resistance and metabolic disorders. Despite intense investigations and establishment of both preventive and therapeutic strategies, insulin resistance–associated metabolic diseases such as type 2 diabetes, obesity, and nonalcoholic fatty liver disease have reached alarming proportions worldwide (Angulo 2002; Ford et al. 2004; Zimmet et al. 2001). By 2015, the World Health Organization (WHO) estimates that 1.5 billion people will be overweight and that 338 million people will die from chronic diseases such as diabetes and heart disease (WHO 2005). Although physical inactivity and regular intake of high-energy diets are recognized contributors (Hill and Peters 1998; Roberts and Barnard 2005), these lifestyle factors can only partially explain the explosive and uncontrolled global increase in metabolic diseases. Recently, the development of insulin resistance and inflammation was found to be exacerbated in humans and animals exposed to air pollution (Kelishadi et al. 2009; Sun et al. 2009). Furthermore, the widespread environmental contaminant bisphenol A was reported to impair pancreatic beta cells and trigger insulin resistance (Alonso-Magdalena et al. 2006). Our data, together with the finding that type 2 diabetics accumulate significant body burdens of POPs (Lee et al. 2006), provide additional evidence that global environmental pollution contributes to the epidemic of insulin resistance–associated metabolic diseases. Although rats chronically fed the HFC diet for 28 days were exposed to a relatively high intake of organic pollutants, the concentrations of PCDDs/PCDFs and indicator PCBs in adipose tissue of these animals did not exceed those observed in Northern Europeans 40–50 years of age (Kiviranta et al. 2005), thereby indicating that doses of POP exposure sufficient to induce detrimental health effects were not excessive. Whether the exposure to lower levels of POPs would induce similar detrimental effects as those observed in the present study remains to be investigated. Dietary interventions are current strategies to prevent or treat metabolic diseases, and nutritional guidelines are usually based on energy density and glycemic index of the diet; however, the levels of POPs present in food has received less attention. Given that POPs are ubiquitous in food chains (Fisher 1999), such underestimation may interfere with the expected beneficial effects of some dietary recommendations and lead to poor outcomes. For instance, the presence of POPs in food products may, to some extent, explain the conflicting results regarding the protective effects of n-3 polyunsaturated fatty acids against the incidence of myocardial infarction (Guallar et al. 1999; Rissanen et al. 2000). Overall, better understanding of the interactions between POPs and nutrients will help improve nutritional education of patients with insulin resistance syndrome. To protect consumer health, the presence of contaminants in food is internationally regulated. In the European Union legislation, certain POPs including dioxins and dioxin-like PCBs are regulated in foodstuffs (European Union 2006). Risk assessment of these organic pollutants is based on the ability of individual compounds to produce heterogeneous toxic and biological effects through the binding of the aryl hydrocarbon receptor. Interestingly, we found that cultured adipocytes exposed to a PCDF or PCDD mixture have normal insulin action, even though the TEQ of these mixtures could be up to 3,500 times higher than the TEQ of the non-ortho-substituted and mono-ortho- substituted PCB mixtures that impaired insulin action. These findings demonstrate that risk assessment based on WHO TEQs assigned to dioxins and dioxin-like PCBs is unlikely to reflect the risk of insulin resistance and the possible development of metabolic disorders. Although the production of organochlorine pesticides has been restricted since the 1970s, the global production and use of pesticides are poorly controlled (Jorgenson 2001; Nweke and Sanders 2009), and the presence of these environmental chemicals in seafood still remains unregulated in European countries (European Union 2008). Of the POP mixtures tested in vitro, organochlorine pesticides were the most potent disruptors of insulin action. This powerful inhibitory effect of pesticides on insulin action likely explains the common finding emerging from several independent cross-sectional studies reporting an association between type 2 diabetes and the body burdens of p,p′-DDE, oxychlordane, or trans-nonachlor (Lee et al. 2006; Rignell-Hydbom et al. 2007; Turyk et al. 2009). Therefore, widespread pesticide exposure to humans appears to be of particular global concern in relation to public health. We draw two main conclusions from these observations. First, exposure to POPs present in the environment and food chains are capable of causing insulin resistance and impair both lipid and glucose metabolism, thus supporting the notion that these chemicals are potential contributors to the rise in prevalence of insulin resistance and associated disorders (Figure 4). Second, although beneficial, the presence of n-3 polyunsaturated fatty acids in crude salmon oil (in the HFC diet) could not counteract the deleterious metabolic effects induced by POP exposure. Altogether, our data provide novel insights regarding the ability of POPs to mediate insulin resistance– associated metabolic abnormalities and provide solid evidence reinforcing the importance of international agreements to limit the release of POPs to minimize public health risks." |
#20
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Exposure to Chemical Pollutants Increases Fat
On Jul 9, 6:08*pm, montygraham wrote:
Another instance where they should have had two other groups of rats, both of which would be fed coconut oil rather than fish oil, one would get the POPs and one would not. *My guess is that they are not familiar with the relevant literature, because it suggests that coconut oil and POPs might not present any major problem, unlike fish oil and POPs. *If so, it would have been yet another good demonstration of the apparent dangers of fish oil. quack quack Warning::: Monty1945 is a certified nut case pretending to have medical credentials. He posts across the Internet, trolling for victims and recommends a diet high saturated fat content for a healthy lifestyle, and as a cure for disease. He denies the existence of AID's. In addition, "Dr Monty" by admission in usenet, uses his body for experimental purposes, the results, being as they are, a completely dysfunctional brain pattern, probably secondary to the stoke he has acquired by following his own medical advice. He's also been know to have two way conversations with his AM/FM radio and to hound professional athletes. Anything he posts needs to be viewed as the rantings of a brain damaged adult limited to 24/7 skill nursing care. thus speakith Monty the troll: QUOTE Did you read my recent post here, "Using basic logic to understand "HIV/AIDS."" ? They have abandoned logic, even at the most basic level. We are beyond the Emperor's New Clothes now. In this case, the "Emperor" has no kingdom, aside from the asylum and his fellow inmates, whom he calls his "subjects." Like all periods of fanaticism, this one will come to an end at some point, and historians like myself will write about it in very similar terms as they do now the witchcraft fears of the sixteenth and seventeenth centuries in Europe. Being heavily "invested" in a notion is quite similar to insanity, and many of us realize this in politics these days, but when it comes to what is considered "science," it is much easier to convince the public that "white is black" and "black is white." Thus, it will take longer for the deadly "HIV=AIDS=DEATH" house of cards to crumble than it does for incompetent, ideological-minded politicians to be voted out of office. If you have yet to do so, I explain what the best explanation for "HIV/AIDS" is on my web site: http://groups.msn.com/TheScientificDebateForum-/ I quote the "virus hunters" directly, and I also cite numerous studies from the scientific literature. /QUOTE |
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