Oral exposure to BDE-209 modulates metastatic spread of melanoma in C57BL/6 mice inoculated with B16-F10 cells.

Polybrominated diphenyl ethers (PBDEs) are brominated, persistent and bioaccumulative flame retardants widely used in the manufacture of plastic products. Decabromodiphenyl ether (BDE-209) is the most prevalent PBDE in the atmosphere and found in human blood, breast milk and umbilical cord. In vitro studies showed that BDE-209 interferes with murine melanoma cells (B16F10), modulating cell death rates, proliferation and migration, important events for cancer progression. In order to evaluate if BDE-209 modulates metastasis formation in murine models, C57BL/6 mice were exposed to BDE-209 (0.08, 0.8 and 8 µg/kg) via gavage (5-day intervals for 45 days) (9 doses in total). Then, mice were inoculated with melanoma cells (B16-F10) at caudal vein receiving 4 additional doses of BDE-209. At 20th day post-cell inoculation, blood, lung, liver, kidney and brain were sampled for hematological, biochemical and morphological analyses. The slightly higher levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the blood and pro-oxidant state in the liver of BDE-exposed mice indicated liver damage. Although the in vivo approach is for metastasis formation in the lung, they were unexpectedly observed in non-target organs (liver, brain, kidney and gonads). The similarity test showed high proximity among individuals from the control and a dissimilarity index between the control and exposed groups. The present data corroborate the known hepatotoxicity of BDE-209 to mice (C57BL/6) and demonstrate for the first time the increase of metastatic dissemination of B16F10 cells in vivo due to previous and continuous BDE-209 exposure, revealing possible implications of this organic compound with melanoma malignancy related traits.

Metabolical shifts towards alternative BTEX biodegradation intermediates induced by perfluorinated compounds in firefighting foams.

The type and concentration of perfluorinated compounds (PFCs) can induce different types of enzymes and promote alternate patterns of BTEX transformation. However, it is not known how the presence of active fluorocarbon-degrading microbial populations affects the transformation of BTEX. In addition to chemical analysis at the molecular level, our research approached the aqueous film forming fire-fighting foams (AFFF) and BTEX co-contamination at a large-scale with respirometers to quantify the total microbial metabolism of soil via CO2 output levels. The intended outcome of this research was to obtain and characterize shifts in BTEX degradation at a set realistic environmental condition while measuring byproducts and CO2 production. Both methodologies complimentarily provided an in-depth knowledge of the environmental behavior of fire-fighting foams. The biodegradation was monitored using headspace sampling and two types of gas chromatography: thermal conductivity detector and flame ionization detector. Headspace samples were periodically withdrawn for BTEX biodegradation and CO2 production analysis. Our research suggests the discovery of an altered metabolic pathway in aromatic hydrocarbons biodegradation that is directly affected by fluorinated substances. The fluorinated compounds affected the BTEX biodegradation kinetics, as PFCs may contribute to a shift in styrene and catechol concentrations in co-contamination scenarios. A faster production of styrene and catechol was detected. Catechol is also rapidly consumed, thus undergoing further metabolic stages earlier under the presence of PFCs. The release of AFFF compounds not only changes byproducts output but also drastically disturbs the soil microbiota according to the highly variable CO2 yields. Therefore, we observed a high sensitivity of microbial consortia due to PFCs in the AFFF formulation, therefore shifting their BTEX degradation routes in terms of intermediate products concentration.