Polychlorinated biphenyls and links to cardiovascular disease

Perkins, Jordan T.; Petriello, Michael C.; Newsome, Bradley J.; Hennig, Bernhard

doi:10.1007/s11356-015-4479-6

Cited by 98 publications

(58 citation statements)

References 188 publications

(225 reference statements)

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“…Indeed, although restriction of fish intake other than perhaps for pregnant/breastfeeding women is not universally advised, serious questions remain unanswered and are not inconsequential in CV patients [107][108][109].…”

Section: Resultsmentioning

confidence: 99%

n-3 Polyunsaturated Fatty Acids and Cardiovascular Disease: Principles, Practices, Pitfalls, and Promises - A Contemporary Review

Kones¹,

Howell²,

Rumana³

2017

Med Princ Pract

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Amidst voluminous literature, inconsistencies and opposing results have confused rather than clarified cardiologists' ability to assess the potential benefits of n-3 polyunsaturated fatty acids (n-3 PUFA). In perspective, there are common themes that emerge from n-3 PUFA studies, even as imperfect as they may be. The approach taken was to identify and unite these themes into a manageable, cohesive, evidence-based, yet useful synthesis. In all reviews and meta-analyses, the selection of component studies and assumptions influences outcomes. This overarching principle must be combined with the totality of the data, particularly when evidence is incompletely understood and gaps in knowledge must be bridged. Both the older literature and the most recent rigorous meta-analyses indicate that n-3 PUFA are highly pleiotropic agents with many documented positive physiological effects. Concordance among preclinical, observational, randomized clinical trials and meta-analyses is impressive. These agents have modest, statistically significant benefits which accrue over time. Given their favorable safety profile, a risk reduction of about 10% justifies their potential use in cardiovascular disease.

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Section: Resultsmentioning

confidence: 99%

n-3 Polyunsaturated Fatty Acids and Cardiovascular Disease: Principles, Practices, Pitfalls, and Promises - A Contemporary Review

Kones¹,

Howell²,

Rumana³

2017

Med Princ Pract

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“…Besides the involvement of immune cells in the development of atherosclerosis [6], the endothelial cell also participates and its dysfunction is a critical underlying cause of CVD [7]. Epidemiological studies provide substantial evidence that the pathology of CVD is associated with exposure to environmental pollutants, such as polychlorinated biphenyls (PCBs) [8–10]. Importantly, PCB exposure is believed to cause vascular inflammation through expression of several inflammatory markers, cytokines and adhesion molecules [11–13].…”

Section: Introductionmentioning

confidence: 99%

EGCG prevents PCB-126-induced endothelial cell inflammation via epigenetic modifications of NF-κB target genes in human endothelial cells

Liu

Perkins

Hennig

2016

The Journal of Nutritional Biochemistry

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Anti-inflammatory polyphenols, such as epigallocatechin-3-gallate (EGCG), have been shown to protect against the toxicity of environmental pollutants. It is well known that bioactive food compounds such as polyphenols may exert their protection by modulating inflammatory pathways regulated through nuclear factor-kappa B (NF-κB) signaling. EGCG has been reported to inhibit NF-κB activation. We hypothesize that EGCG can protect against PCB-induced endothelial inflammation in part through epigenetic regulation of NF-kB-regulated inflammatory genes. In order to test this hypothesis, human endothelial cells (EA.hy926) were exposed to physiologically relevant levels of coplanar PCB 126 and/or 15 or 30 μM of EGCG, followed by quantification of NF-kB subunit p65, histone acetyltransferase (HAT) p300 and histone deacetylases (HDACs) accumulation through ChIP assay in the promotor region of inflammatory genes. In addition, the enrichment of the acetylated H3 (ac-H3) was also quantified. PCB 126 exposure increased the expression of vascular inflammatory mediators, including interleukin (IL)-6, C-reactive protein (CRP), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and IL-1α/β, which were prevented by pre-treatment with EGCG. This inhibitory effect by EGCG correlated with abolished nuclear import of p65, decreased chromatin binding of p65 and p300, as well as increased chromatin binding of HDAC1/2. Furthermore, EGCG induced hypo-acetylation of H3, which accounts for deactivation of downstream genes. These data suggest that EGCG-induced epigenetic modifications can decrease PCB-induced vascular toxicity.

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“…In summary, epidemiological studies have linked exposure to POPs, such as PCBs, with an increased risk of developing diabetes, hypertension, and obesity, all of which lead to onset and progression of CVD [16]. Emerging evidence now suggests that green tea with its anti-inflammatory and anti-oxidative properties can decrease vascular toxicity and provide protection against PCBs-induced vascular toxicities.…”

Section: Green Tea Modulates Toxicities Associated With Pcbsmentioning

confidence: 99%

“…Epidemiological evidence now implicates exposure to PCBs in an increased risk of developing diabetes, hypertension, and obesity, all of which are clinically relevant to the onset and progression of cardiovascular disease. It is also suggested that PCBs exert their cardiovascular toxicity via additional mechanisms, including induction of chronic oxidative stress, inflammation, and endocrine disruption [16]. …”

Section: Introductionmentioning

confidence: 99%

Therapeutic properties of green tea against environmental insults

Chen¹,

Zhao

et al. 2017

The Journal of Nutritional Biochemistry

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Pesticides, smoke, mycotoxins, polychlorinated biphenyls, and arsenic are the most common environmental toxins and toxicants to humans. These toxins and toxicants may impact on human health at the molecular (DNA, RNA, or protein), organelle (mitochondria, lysosome, or membranes), cellular (growth inhibition or cell death), tissue, organ, and systemic levels. Formation of reactive radicals, lipid peroxidation, inflammation, genotoxicity, hepatotoxicity, embryotoxicity, neurological alterations, apoptosis, and carcinogenic events are some of the mechanisms mediating the toxic effects of the environmental toxins and toxicants. Green tea, the non-oxidized and non-fermented form of tea that contains several polyphenols, including green tea catechins, exhibits protective effects against these environmental toxins and toxicants in preclinical studies and to a much-limited extent, in clinical trials. The protective effects are collectively mediated by antioxidant, anti-inflammatory, anti-mutagenic, hepato- and neuroprotective, and anti-carcinogenic activities. In addition, green tea modulates signaling pathway including NFκB and ERK pathways, preserves mitochondrial membrane potential, inhibits caspase-3 activity, down-regulates pro-apoptotic proteins, and induces the phase II detoxifying pathway. The bioavailability and metabolism of green tea and its protective effects against environmental insults induced by pesticides, smoke, mycotoxins, polychlorinated biphenyls, and arsenic are reviewed in this paper. Future studies with emphasis on clinical trials should identify biomarkers of green tea intake, examine the mechanisms of action of green tea polyphenols, and investigate potential interactions of green tea with other toxicant-modulating dietary factors.

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Polychlorinated biphenyls and links to cardiovascular disease

Cited by 98 publications

References 188 publications

n-3 Polyunsaturated Fatty Acids and Cardiovascular Disease: Principles, Practices, Pitfalls, and Promises - A Contemporary Review

n-3 Polyunsaturated Fatty Acids and Cardiovascular Disease: Principles, Practices, Pitfalls, and Promises - A Contemporary Review

EGCG prevents PCB-126-induced endothelial cell inflammation via epigenetic modifications of NF-κB target genes in human endothelial cells

Therapeutic properties of green tea against environmental insults

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