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1.
Mar Drugs ; 18(1)2019 Dec 18.
Artigo em Inglês | MEDLINE | ID: mdl-31861403

RESUMO

Marine microalgae are known to be a source of bioactive molecules of interest to human health, such as n-3 polyunsaturated fatty acids (n-3 PUFAs) and carotenoids. The fact that some of these natural compounds are known to exhibit anti-inflammatory, antioxidant, anti-proliferative, and apoptosis-inducing effects, demonstrates their potential use in preventing cancers and cardiovascular diseases (CVDs). Benzo[a]pyrene (B[a]P), a polycyclic aromatic hydrocarbon (PAH), is an ubiquitous environmental pollutant known to contribute to the development or aggravation of human diseases, such as cancer, CVDs, and immune dysfunction. Most of these deleterious effects are related to the activation of the polycyclic aromatic hydrocarbon receptor (AhR). In this context, two ethanolic microalgal extracts with concentrations of 0.1 to 5 µg/mL are tested, Ostreoccoccus tauri (OT) and Phaeodactylum tricornutum (PT), in order to evaluate and compare their potential effects towards B[a]P-induced toxicity in endothelial HMEC-1 cells. Our results indicate that the OT extract can influence the toxicity of B[a]P. Indeed, apoptosis and the production of extracellular vesicles were decreased, likely through the reduction of the expression of CYP1A1, a B[a]P bioactivation enzyme. Furthermore, the B[a]P-induced expression of the inflammatory cytokines IL-8 and IL1-ß was reduced. The PT extract only inhibited the expression of the B[a]P-induced cytokine IL-8 expression. The OT extract therefore seems to be a good candidate for counteracting the B[a]P toxicity.


Assuntos
Benzo(a)pireno/toxicidade , Produtos Biológicos/farmacologia , Microalgas/química , Apoptose/efeitos dos fármacos , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Citocromo P-450 CYP1A1/metabolismo , Citocinas/efeitos dos fármacos , Células Endoteliais , Vesículas Extracelulares/efeitos dos fármacos , Vesículas Extracelulares/ultraestrutura , Humanos , Oceanos e Mares
2.
FEBS Lett ; 579(9): 1904-10, 2005 Mar 28.
Artigo em Inglês | MEDLINE | ID: mdl-15792794

RESUMO

Polycyclic aromatic hydrocarbons (PAHs) such as benzo(a)pyrene (BP) are toxic environmental contaminants known to enhance production of pro-inflammatory cytokines such as IL-1beta. The present study was designed in order to determine whether TNFalpha, another cytokine acting in inflammation, may also constitute a target for these chemicals. Both TNFalpha mRNA and TNFalpha secretion levels were found to be enhanced in human BP-treated macrophages. Dioxin, a contaminant activating the aryl hydrocarbon receptor (AhR) like PAHs, was also shown to increase TNFalpha expression. BP-mediated TNFalpha induction was however not suppressed by AhR antagonists, making unlikely the involvement of the typical AhR signalling pathway. BP-exposure of macrophages did not enhance NF-kappaB DNA binding activity, but it activated the MAP kinase ERK1/2. In addition, the use of chemical inhibitors of extracellular signal-regulated protein kinase (ERK) activation fully abrogated induction of TNFalpha production in BP-treated macrophages. These data likely indicate that PAHs enhance TNFalpha expression in human macrophages through an ERK-related mechanism. Such a regulation may contribute to confer pro-inflammatory properties to these widely-distributed environmental contaminants.


Assuntos
Benzo(a)pireno/farmacologia , Poluentes Ambientais/farmacologia , MAP Quinases Reguladas por Sinal Extracelular/fisiologia , Macrófagos/efeitos dos fármacos , Fator de Necrose Tumoral alfa/metabolismo , Butadienos/farmacologia , Células Cultivadas , Proteínas de Ligação a DNA/metabolismo , MAP Quinases Reguladas por Sinal Extracelular/antagonistas & inibidores , Flavonoides/farmacologia , Expressão Gênica/efeitos dos fármacos , Humanos , Macrófagos/enzimologia , Macrófagos/imunologia , NF-kappa B/metabolismo , Nitrilas/farmacologia , Dibenzodioxinas Policloradas/farmacologia , Inibidores de Proteínas Quinases/farmacologia , RNA Mensageiro/análise , RNA Mensageiro/metabolismo , Receptores de Hidrocarboneto Arílico/antagonistas & inibidores , Fator de Necrose Tumoral alfa/genética , Regulação para Cima
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