Changing ratios of omega-6 to omega-3 fatty acids can differentially modulate polychlorinated biphenyl toxicity in endothelial cells

Wang, Lei; Reiterer, Gudrun; Toborek, Michał; Hennig, Bernhard

doi:10.1016/j.cbi.2007.11.003

Cited by 28 publications

(24 citation statements)

References 47 publications

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“…In this respect, in a recent study, Alegría-Torres et al (Frigo et al, 2004;Kim et al, 2004). Similar findings were found for PCBs (Bezdecny et al, 2007;Glauert et al, 2008;Myhre et al, 2009;Wang et al, 2008). In line with the mechanism proposed by Champion et al (2013), our data showed that the over-expression of AhR was dependent on the TNF induced by DDE and PCB 153.…”

Section: Discussionsupporting

confidence: 91%

“…Those findings indicated that AhR expression in FLSs was stimulated in the presence of TNF, similar to our results here. Taking into account that data and our own, we hypothesize that TNF induced by DDE and PCB 153 (Alegría-Torres et al 2009; Cárdenas-González et al, 2013), likely via an NF-B pathway (Bezdecny et al, 2007;Frigo et al, 2004;Glauert et al, 2008;Kim et al, 2004;Myhre et al, 2009;Wang et al, 2008), was able to induce AhR mRNA expression.…”

Section: Discussionmentioning

confidence: 62%

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DDE and PCB 153 independently induce aryl hydrocarbon receptor (AhR) expression in peripheral blood mononuclear cells

Gaspar-Ramírez

Pérez‐Vázquez

Salgado‐Bustamante³

et al. 2014

Journal of Immunotoxicology

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Recent studies have demonstrated that compounds inducing pro-inflammatory cytokines enhance AhR expression. The aim of this study was 2-fold: (1) to determine if two pro-inflammatory compounds, dichlorodiphenyldichloroethylene (DDE) and 2,2 0 ,4,4 0 ,5,5 0 -hexa-chlorobiphenyl (PCB 153), independently affect AhR gene expression in peripheral blood mononuclear cells (PBMC); and (2) if affected, to determine whether the mechanism involved was due to AhR activation or to a pro-inflammatory effect of the chemicals. PBMC isolated from healthy individuals were incubated in the presence of DDE (10 mg/ml) and PCB 153 (20 ng/ml) over time and AhR and CYP1A1 expression was assessed with a real-time PCR technique. The results indicated there was over-expression of the AhR mRNA in PBMC when the cells were treated with DDE and PCB 153. No changes in expression levels of CYP1A1 mRNA were found. Importantly, when the cells were exposed to DDE and PCB 153 in the presence of an antagonist of tumor necrosis factor (TNF)-, the over-expression of AhR was abolished; as expected, the expression of CYP1A1 was unaffected. In conclusion, these studies demonstrated for the first time an increment of AhR expression ''in vitro'' in PBMC treated with two pro-inflammatory environmental pollutants, DDE and PCB153. Moreover, the over-expression of AhR was dependent of TNF induced by DDE and PCB 153 and was independent of AhR activation.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 62%

DDE and PCB 153 independently induce aryl hydrocarbon receptor (AhR) expression in peripheral blood mononuclear cells

Gaspar-Ramírez

Pérez‐Vázquez

Salgado‐Bustamante³

et al. 2014

Journal of Immunotoxicology

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“…cultured hepatocytes (Palanisamy et al, 2015;Turkez et al, 2011b) and that a higher ratio of n-3/n-6 PUFAs can reduce oxidative stress and inflammation induced by the dioxin-like polychlorinated biphenyl, PCB77, in cultured endothelial cells (Wang et al, 2008). Additionally, both EPA and DHA protect against TCDD-induced oxidative stress and hepatic and renal injury in rats in vivo (Palaniswamy et al, 2014;Turkez et al, 2011a).…”

Section: Discussionmentioning

confidence: 99%

Dietary Omega-3 Polyunsaturated Fatty Acids Prevent Vascular Dysfunction and Attenuate Cytochrome P4501A1 Expression by 2,3,7,8-Tetrachlorodibenzo-P-Dioxin

et al. 2016

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Omega-3 polyunsaturated fatty acids (n-3 PUFAs) found in fish protect against cardiovascular morbidity and mortality; however, many individuals avoid fish consumption due to concerns about pollutants. We tested the hypothesis that n-3 PUFAs would prevent vascular dysfunction induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). C57Bl/6 male mice were fed a chow or n-3 PUFA diet for 10 weeks and were exposed to vehicle or 300 ng/kg/d TCDD during the final 2 weeks on each diet. Aortic vasoconstriction mediated by arachidonic acid (AA) 6 SKF525 (P450 inhibitor) or SQ29548 (thromboxane/ prostanoid [TP] receptor antagonist) was assessed. RBC fatty acids and expression of n-3 and n-6 PUFA metabolites were analyzed. Cytochrome P4501A1 (CYP1A1), CYP1B1, and aryl hydrocarbon receptor (AHR) expression was measured. TCDD significantly increased AA-mediated vasoconstriction on a chow diet by increasing the contribution of P450s and TP receptor to the constriction response. In contrast, the n-3 PUFA diet prevented the TCDD-induced increase in AA vasoconstriction and normalized the contribution of P450s and TP receptor. Although TCDD increased the levels of AA vasoconstrictors on the chow diet, this increase was prevent by the n-3 PUFA diet. Additionally, the n-3 PUFA diet significantly increased the levels of n-3 PUFA-derived vasodilators and TCDD increased these levels further. Interestingly, the n-3 PUFA diet significantly attenuated CYP1A1 induction by TCDD without a significant effect on AHR expression. These data suggest that n-3 PUFAs can prevent TCDD-induced vascular dysfunction by decreasing vasoconstrictors, increasing vasodilators, and attenuating CYP1A1 induction, which has been shown previously to contribute to TCDD-induced vascular dysfunction.

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“…The uptake of polychlorinated biphenyls (PCBs) by endothelial cells has been shown to be increased in the presence of linoleic acid (141), and it has been suggested that PCBs activate endothelial cells by mechanisms involving caveolae (90). It is possible that PCBs accumulate in the caveolae of endothelial cells and somehow interact with specific fatty acids since linoleic acid amplified, whereas α-linolenic acid protected against, PCB-induced endothelial activation (159,164). Oily fish containing longchain n-3 PUFAs could potentially be contaminated with organic pollutants and thus represent a food group that has substantial health benefits as well as possible risks (59).…”

Section: Fatty Acids Lipid Rafts and Environmental Toxicity In Endomentioning

confidence: 99%

The Nutritional Significance of Lipid Rafts

Yaqoob

2009

Annu. Rev. Nutr.

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The structure, size, stability, and functionality of lipid rafts are still in debate, but recent techniques allowing direct visualization have characterized them in a wide range of cell types. Lipid rafts are potentially modifiable by diet, particularly (but not exclusively) by dietary fatty acids. However, it is not clear whether dietary polyunsaturated fatty acids (PUFAs) are incorporated into raft lipids or whether their low affinity to cholesterol disallows this and causes phase separation from rafts and displacement of raft proteins. This review examines the potential for dietary modification of raft structure and function in the immune system, brain and retinal tissue, the gut, and in cancer cells. Although there is increasing evidence to suggest that membrane microdomains, and their modulation, have an impact in health and disease, it is too early to judge whether modulation of lipid rafts is responsible for the immunomodulatory effects of n-3 PUFA. In addition to dietary fatty acids, gangliosides and cholesterol may also modulate microdomains in a number of tissues, and recent work has highlighted sphingolipids in membrane microdomains as potential targets for inhibition of tumor growth by n-3 PUFA. The roles of fatty acids and gangliosides in cognitive development, age-related cognitive decline, psychiatric disorders, and Alzheimer's disease are poorly understood and require clarification, particularly with respect to the contribution of lipid rafts. The roles of lipid rafts in cancer, in microbial pathogenesis, and in insulin resistance are only just emerging, but compelling evidence indicates the growing importance of membrane microdomains in health and disease.

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Changing ratios of omega-6 to omega-3 fatty acids can differentially modulate polychlorinated biphenyl toxicity in endothelial cells

Cited by 28 publications

References 47 publications

DDE and PCB 153 independently induce aryl hydrocarbon receptor (AhR) expression in peripheral blood mononuclear cells

DDE and PCB 153 independently induce aryl hydrocarbon receptor (AhR) expression in peripheral blood mononuclear cells

Dietary Omega-3 Polyunsaturated Fatty Acids Prevent Vascular Dysfunction and Attenuate Cytochrome P4501A1 Expression by 2,3,7,8-Tetrachlorodibenzo-P-Dioxin

The Nutritional Significance of Lipid Rafts

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