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Exposure to Chemical Pollutants Increases Fat
http://www.scientificamerican.com/ar...tants-fat-diet
Study Finds Exposure to Chemical Pollutants Increases Fat Rats exposed to high levels of chemical pollutants in fish oil could not regulate fat properly By Sara Goodman | January 15, 2010 | 8 FAT CHEMICAL: A chemical found in fatty foods could be sentencing people to metabolic problems such as obesity and fatigue. Researchers have for the first time found a connection between exposure to certain chemicals and insulin resistance, according to a study published in the online edition of Environmental Health Perspectives. A group of European scientists examined whether exposure to persistent organic pollutants (POPs) contributed to insulin resistance, which has been increasing around the world. More than 25 percent of U.S. adults suffer from metabolic conditions stemming from insulin resistance that include fatigue, obesity and difficulty regulating blood levels of fat and sugar. Researchers fed rats a high-fat diet of either crude or refined fish oil from farmed Atlantic salmon over 28 days. The crude fish oil contained average levels of POPs that people are exposed to through fish consumption, while the refined oil contained none. Both had equal fat levels. They found that rats exposed to the crude fish oil developed belly fat and could not regulate fat properly. They had higher levels of cholesterol and several fatty acids in their livers. Those exposed to the refined fish oil experienced none of those symptoms. Researchers said the findings provide "compelling evidence" of a causal relationship between POP exposure common in the food chain and insulin resistance, and highlight the need to understand the interactions of POPs and fat-containing foods such as fish, dairy products and meat. How to deal with POPs is particularly challenging because they persist in the environment for long periods and can build up in animals' tissues. The 2001 Stockholm Convention, which the United States has ratified but not signed, lists and bans numerous POPs from manufacture and use. The researchers say their evidence reinforces the need to have international agreements aimed at limiting the release of POPs into the environment in an effort to protect public health. |
#2
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Exposure to Chemical Pollutants Increases Fat
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. |
#3
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Exposure to Chemical Pollutants Increases Fat
On Jul 9, 5:08*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. Some POPs alter cells via a non-ROS mechanism. Some POPs produce reactive quinones that bind DNA. POPs tend to hyperactive Phase I enzymes which tend to produce more reactive chemicals so that they can by bound and excreted by Phase II enzymes/anti-oxidants. Reducing excess iron, proteins in addition to polyunsaturated oils should help also. |
#4
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Exposure to Chemical Pollutants Increases Fat
In article
, jay wrote: On Jul 9, 5:08*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. Some POPs alter cells via a non-ROS mechanism. Some POPs produce reactive quinones that bind DNA. POPs tend to hyperactive Phase I enzymes which tend to produce more reactive chemicals so that they can by bound and excreted by Phase II enzymes/anti-oxidants. Reducing excess iron, proteins in addition to polyunsaturated oils should help also. Do you have a citation for the above? -- - 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-/ |
#5
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Exposure to Chemical Pollutants Increases Fat
... 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 |
#6
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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-/ |
#7
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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 |
#8
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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 |
#9
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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 |
#10
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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 |
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