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From: ironjustice on 28 Aug 2008 20:05 http://tinyurl.com/6n92gm Oxidative stress and nutritional prevention in autoimmune rheumatic diseases Samir G. Sukkar *, Edoardo Rossia,bDietetics and Clinical Nutrition Unit, University-Hospital San Martino, Largo Rosanna Benzi 10, Genoa, ItalyaDepartment of Haematology, University-Hospital San Martino, Largo Rosanna Benzi 10, Genoa, Italy ● The evaluation of oxidative stress and of nutritional intake is mandatory in the clinical approach of patients affected by autoimmune rheumatic diseases. Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk
From: jay on 28 Aug 2008 21:15 > Oxidative stress and nutritional prevention > in autoimmune rheumatic diseases A role for the aryl hydrocarbon receptor and the dioxin TCDD in rheumatoid arthritis. OBJECTIVE: Environmental factors are involved in RA pathogenesis and epidemiological studies have suggested that smoking is an environmental risk factor for RA. The 2,3,7,8-tetrachlorodibenzo-p- dioxin (TCDD) is one of the major toxic components in cigarettes. To clarify the biological effects of smoking in RA, we investigated the role of TCDD in RA pathogenesis. ...CONCLUSION: TNF-alpha activates AhR expression in RA synovial tissue, and that cigarette smoking and exposure to TCDD enhances RA inflammatory processes. TCDD induces inflammatory cytokines via its association with AhR, resulting in stimulation of the NF-kappaB and ERK signalling cascades. Thus TCDD exposure, such as smoking exacerbates RA pathophysiology. PMID: 18617548 Polycyclic aromatic hydrocarbon increases mRNA level for interleukin 1 beta in human fibroblast-like synoviocyte line via aryl hydrocarbon receptor. Rheumatoid arthritis (RA) is characterized by proliferation of synoviocytes that produce proinflammatory cytokines, which is implicated in the pathogenesis of the disease ... Benzo[a]pyrene (B[a]P) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) also up- regulated mRNA level of IL-1beta in the cells via AhR. As PAHs are much contained in cigarette smoke, these findings provide the possible basis for epidemiological studies indicating a strong association between heavy cigarette smoking and outcome of RA. PMID: 14993811 Positive associations of serum concentration of polychlorinated biphenyls or organochlorine pesticides with self-reported arthritis, especially rheumatoid type, in women. BACKGROUND: Persistent organic pollutants (POPs) can influence the immune system, possibly increasing the risk of rheumatoid arthritis (RA). In addition, as metabolic change due to obesity has been proposed as one mechanism of osteoarthritis (OA), POPs stored in adipose tissue may be also associated with OA. OBJECTIVE: Our goal in this study was to examine associations of background exposure to POPs with arthritis among the general population. DESIGN: We investigated cross-sectional associations of serum POPs concentrations with the prevalence of self-reported arthritis in 1,721 adults >/= 20 years of age in the National Health and Nutrition Examination Survey 1999-2002. ...CONCLUSIONS: The possibility that background exposure to PCBs may be involved in pathogenesis of arthritis, especially RA, in women should be investigated in prospective studies.PMID: 17589595 Dioxin exposure and non-malignant health effects: a mortality study. OBJECTIVE: To investigate, in a population heavily exposed to 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD), the possible unusual occurrence of diseases other than cancer. METHODS: Five year extension of the follow up of the cohort involved in the Seveso accident. Soil measurements identified three exposure zones: (A) highest contamination, (B) substantial, and (R) low but higher than background contamination. Blood TCDD measurements, although limited in number, confirmed zone exposure ranking. The 15 year mortality in the exposed cohort was compared with that of a large population in the surrounding non- contaminated territory. Relative risks (RRs) and 95% confidence intervals (95% CIs) were estimated with Poisson regression techniques. RESULTS: The already noted increased occurrence of cardiovascular deaths was confirmed, in particular in zone A, among males for chronic ischaemic heart disease (five deaths, RR 3.0, 95% CI 1.2 to 7.3), and among females for hypertensive disease (three deaths, RR 3.6, 95% CI 1.2 to 11.4) and chronic RHEUMATIC heart disease. Novel findings were the increase of chronic obstructive pulmonary disease, most notably among males in zone A (four deaths, RR 3.7, 95% CI 1.4 to 9.9) and females in zone B (seven deaths, RR 2.4, 95% CI 1.1 to 5.1); and from diabetes, which was significantly increased in females in zone B (13 deaths, RR 1.9, 95% CI 1.1 to 3.2). In zone R, chronic ischaemic heart disease (males and females), hypertension (females), and diabetes (females) showed less pronounced, although significant excesses. CONCLUSIONS: As well as high TCDD exposure, the accident caused a severe burden of strain in the population. Both these factors might have contributed to the noted increased risks (in particular, circulatory and respiratory). The cardiovascular and immune toxicity of TCDD, as well as its complex interaction with the endocrine system, might be relevant to the explanations of these findings. These results, although not conclusive, concur with previous data in suggesting cardiopulmonary and endocrine effects in humans highly exposed to TCDD. PMID: 9614398 Oxidative stress induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is one of the most potent toxins and tumor promoters known to man. It is prototypical of many halogenated polycyclic hydrocarbons that occur as environmental contaminants. Pathologic lesions produced by these compounds are mediated by an intracellular receptor protein called the TCDD (Ah) receptor which functions as a trans-acting effector of gene expression. However, the ultimate posttranslational pathways and mechanisms involved in the expression of the toxic manifestations of TCDD have received little attention and remain unclear, yet constitute an important segment in our understanding of the overall mechanism of action of TCDD. Recent studies have demonstrated that an oxidative stress occurs in various tissues of TCDD-treated animals. Evidence indicating production of an oxidative stress by TCDD in rodents is reviewed and includes:enhanced in vitro and in vivo hepatic and extrahepatic lipid peroxidation; increased hepatic and macrophage DNA damage; increased urinary excretion of malondialdehyde; decreased hepatic membrane fluidity; increased production of superoxide anion by peritoneal macrophage; and decreased glutathione, nonprotein sulfhydryl, and NADPH contents in liver. The potential role of reactive oxygen species in tumor promotion by TCDD is discussed. Possible sources and mechanisms of production of reactive oxygen species in response to TCDD are considered in light of current information. Evidence demonstrating the involvement of iron in TCDD- induced formation of reactive oxygen species and DNA damage is reviewed. Oxidative damage may contribute to many of the toxic responses produced by TCDD and its bioisosteres, and may be common to most of the tissue-damaging effects. PMID: 2210442
From: ironjustice on 28 Aug 2008 22:09 On Aug 28, 6:15 pm, jay <jaym1...(a)hotmail.com> wrote:Oxidative damage << Jay .. agrees .. http://tinyurl.com/6n92gm Oxidative stress and nutritional prevention in autoimmune rheumatic diseases Samir G. Sukkar *, Edoardo Rossia,bDietetics and Clinical Nutrition Unit, University-Hospital San Martino, Largo Rosanna Benzi 10, Genoa, ItalyaDepartment of Haematology, University-Hospital San Martino, Largo Rosanna Benzi 10, Genoa, Italy ● The evaluation of oxidative stress and of nutritional intake is mandatory in the clinical approach of patients affected by autoimmune rheumatic diseases. Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/634q5a Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk
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