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Omega-3 supplementation on inflammatory markers in patients with chronic Chagas cardiomyopathy: a randomized clinical study.

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BACKGROUND Several studies have been focusing on the effect of omega-3 polyunsaturated fatty acids on modulation of inflammatory markers in several cardiopathies. Although immunoregulatory dysfunction has been associated to the chronic cardiac involvement in Chagas disease, there is no study

BPA-induced DNA hypermethylation of the master mitochondrial gene PGC-1α contributes to cardiomyopathy in male rats.

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Implication of environmental endocrine disruptors, such as bisphenol A (BPA), on the development of cardiopathy has been poorly investigated. The aim of the study was to investigate the effects of long-term exposure to BPA at the reference dose on the myocardium of rats, and the underlying

Recirculating, retrograde heart perfusion according to Langendorff as a tool in the evaluation of drug-induced cardiomyopathy: effects of a high lipid diet.

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A recirculating, retrograde heart perfusion according to Langendorff is described as a method for the evaluation of cardiomyopathy as an untoward side effect of a high lipid diet (addition of 10% and 25% corn oil to rat maintenance feed) in female rats. The use of glucose (5 mM) or palmitate (0.5

Effects of omega-3 polyunsaturated fatty acid supplementation in patients with chronic chagasic cardiomyopathy: study protocol for a randomized controlled trial.

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BACKGROUND Chronic chagasic cardiomyopathy is an inflammatory disease that occurs in approximately 30% of patients infected by the protozoan Trypanosoma cruzi, and it has a profile of high morbidity and mortality. The worst prognosis and the progression of this cardiomyopathy are associated with an

Early developmental 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure decreases chick embryo heart chronotropic response to isoproterenol but not to agents affecting signals downstream of the beta-adrenergic receptor.

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) causes cardiovascular toxicity in laboratory animals, including alteration in several processes in which beta-adrenergic receptor (beta-AR) signaling plays important roles. Thus, our laboratory investigated the effects of TCDD on beta-AR expression and

New aspects in probucol cardioprotection against doxorubicin-induced cardiotoxicity.

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OBJECTIVE Doxorubicin (DOX) is a broad-spectrum anticancer drug with dose-dependent cardiotoxicity. Probucol has been reported to completely prevent DOX-induced cardiomyopathy. The aim of the present study was to determine the possible effect of probucol pretreatment on the pharmacokinetics of DOX

Increase in cardiovascular pathology in female Sprague-Dawley rats following chronic treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3,3',4,4',5-pentachlorobiphenyl.

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The effects of chronic exposure to dioxin (2,3,7,8,-tetrachlorodibenzo-pdioxin [TCDD]) and a dioxin-like compound (3,3',4,4',5-pentachlorobiphenyl [PCB126]) on the cardiovascular system were evaluated in female Harlan Sprague-Dawley rats as part of an ongoing National Toxicology Program

New diet (NTP-2000) for rats in the National Toxicology Program toxicity and carcinogenicity studies.

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Composition of diet may influence growth, diseases, tumor rates, and responses to chemical treatment. Since 1980 the NIH-07 open formula nonpurified diet has been the selected diet for the National Toxicology Program (NTP) toxicity and carcinogenicity studies in rodents. Studies with nonpurified

Toxicology and carcinogenesis studies of a mixture of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (Cas No. 1746-01-6), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF) (Cas No. 57117-31-4), and 3,3',4,4',5-pentachlorobiphenyl (PCB 126) (Cas No. 57465-28-8) in female Harlan Sprague-Dawley rats (gavage studies).

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DIOXIN TOXIC EQUIVALENCY FACTOR EVALUATION OVERVIEW: Polyhalogenated aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) have the ability to bind to and activate the ligand-activated transcription factor, the aryl hydrocarbon receptor (AhR). Structurally related compounds that

Toxicology and carcinogenesis studies of 2,3,4,7,8-pentachlorodibenzofuran (PeCDF) (Cas No. 57117-31-4) in female Harlan Sprague-Dawley rats (gavage studies).

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2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) inhibition of coronary vasculogenesis is mediated, in part, by reduced responsiveness to endogenous angiogenic stimuli, including vascular endothelial growth factor A (VEGF-A).

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BACKGROUND 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exposure prior to chick embryo incubation (GD 0) induces dilated cardiomyopathy, and reduces myocardial hypoxia, vascular endothelial growth factor A (VEGF-A) expression, and coronary vascularization. We investigated whether reduced coronary

NTP Technical Report on the Toxicity Studies of 3,3',4,4'-Tetrachloroazoxybenzene (CAS No. 21232-47-3) Administered by Gavage to F344/N Rats and B6C3F1 Mice.

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3,3',4,4'-Tetrachloroazoxybenzene is not commercially manufactured but is present as a contaminant of 3,4-dichloroaniline and its herbicidal derivative Diuron(R). In addition, environmental contamination occurs when 3,3',4,4'-tetrachloroazoxybenzene is formed by the photolysis and biolysis of

Dietary mustard, rape seed oils and selenium exert distinct effects on serum Se, lipids, peroxidation products and platelet aggregability.

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OBJECTIVE A degenerative cardiomyopathy (DCM) has been observed among mustard oil (MUST) users in China who eat 150 ml/week. Though the condition may be a selenium (Se) deficiency, MUST, rich in erucic acid (22:1), may bear a cardiotoxic or pro-oxidant substrate(s). The purpose of this feeding study

Identification of novel mimicry epitopes for cardiac myosin heavy chain-α that induce autoimmune myocarditis in A/J mice.

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Myocarditis is one cause of sudden cardiac death in young adolescents, and individuals affected with myocarditis can develop dilated cardiomyopathy, a frequent reason for heart transplantation. Exposure to environmental microbes has been suspected in the initiation of heart autoimmunity, but the

Oxidative stress as a mechanism of added sugar-induced cardiovascular disease.

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Added sugars comprising of table sugar, brown sugar, corn syrup, maple syrup, honey, molasses, and other sweeteners in the prepared processed foods and beverages have been implicated in the pathophysiology of cardiovascular diseases. This article deals with the reactive oxygen species (ROS) as a

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