Remediation and Biological Activity of Nano Zero-valent Iron Supported by Biomass Carbon on Soil Contaminated With Polybrominated Diphenyl Ethers

Polybrominated diphenyl ethers (PBDEs) are toxic to humans and can easily accumulate in the environment. Nanoscale zero-valent iron (NZVI) and modified NZVI have been developed to remediate PBDE contamination. However, their degradation in soil systems and their microbial toxicity have not been widely explored. In this study, NZVI supported on biomass carbon was applied to remove decabromodiphenyl ether (BDE-209) from contaminated soil. A removal efficiency of 100% was achieved within 384 h as BDE-209 reacted with 0.10 g/g soil biomass carbon NZVI particles (BC–NZVI) at pH 7.00. The reaction followed pseudo-first-order kinetics, and the BDE-209 removal efficiency increased with increasing BC–NZVI dosage and decreasing initial BDE-209 concentration, pH, and moisture content. Biological activity assays (dehydrogenase activity and soil basal respiration) were conducted to provide a preliminary risk assessment of the BC–NZVI application in BDE-209 contaminated soil. The results demonstrate that BC–NZVI has a strong potential for in situ remediation of organic-contaminated soil.

BDE-209 Becreases the Efficacy of Dacarbazine Treatment for Melanoma in C57BL/6 Mice

Humans are widely exposed to environmental chemical toxicants potentially related to disease susceptibility. Polybrominated diphenyl ethers (PBDEs) present a proven risk associated with cancer, but no studies are related with the tumor progression. The decabromodiphenyl ether (BDE-209) is a flame-retardant detected in human plasma, breast milk and umbilical cord. Melanoma is a skin cancer with high metastatic potential and poor response to therapies. The use of alkylating agents such as dacarbazine is still a common protocol for the treatment of melanoma, mainly in Brazilian Public Health Care System. Recently, we reported the role of BDE-209 on the incidence of melanoma metastasis in different organs of mice after inoculation of B16-F10 cells. In the current study, we describe the effects of BDE-209 on dacarbazine treatment for melanoma. Adult male and female C57BL6 mice were exposed to BDE-209 for 45 days, inoculated with B16-F10 cells and treated with dacarbazine for 21 days (five doses of 40 mg.kg− 1). At 66th day, the animals were euthanized, and the blood, lung, liver, kidney and brain were sampled for hematological, biochemical and metastasis counting analyses. The results showed a decrease of lung metastases in animals treated with dacarbazine and a significant increase in mice previously exposed to BDE-209. Foremost, BDE-209 impaired dacarbazine treatment. These findings demonstrate the effect of BDE-209 and the decreased efficacy of dacarbazine treatment, favoring cancer progression and affecting the disease prognosis.

BDE-209 and TCDD Modulate the Expression and Activity of ATP-Binding Cassette (ABC) Transporters in Murine Melanoma Cells (B16-F1)

Persistent organic pollutants (POPs) may alter tumor cells phenotype, possibly increasing malignancy, but there is a lack of studies investigating the mechanisms by which POPs may affect tumor cells. The ATP-Binding Cassette (ABC) transporter proteins are a widely studied component of drug resistance and tumor progression. We hypothesized that the levels of BDE-209 and TCDD detected in human serum can modulate the gene expression or activity of ATP-binding cassette (ABC) transporters in murine melanoma (B16-F1) cells. In this study, we observed an upregulation of the ABCB1 and ABCC4 (24 h) genes followed by an increased protein activity after BDE-209 15 day-exposure. We also observed that cells exposed to TCDD showed an upregulation of ABCB5, ABCC1 and ABCC4 genes (24 h) and change of protein activity after 15 days of exposure. These findings suggest that BDE-209 and TCDD can regulate the phenotype of B16-F1 cells by interfering with the expression and activity of ATP-binding cassette (ABC) transporters. This investigation revealed that environmental pollutants might intervene and modify cells’ resistance to chemotherapy and cancer prognosis.