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

Brito, Patricia Manuitt; Biscaia, Stellee Marcela Petris; Souza, Tugstênio Lima de; Ramos, Amandia Batscheuer; Leão-Buchir, Joelma; Roque, Aliciane de Almeida; Bellan, Daniel de Lima; Trindade, Edvaldo da Silva; Neto, Francisco Filipak; Ribeiro, Ciro Alberto de Oliveira

doi:10.1016/j.chemosphere.2020.127556

Cited by 12 publications

(6 citation statements)

References 44 publications

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“…The animals exposed to BDE-209 showed larger tumor nodules than those exposed to BDE-209 and treated with dacarbazine. These nodules showed many melanocytic cells and a well-developed blood vessel around them, similarly to detected in the vehicle group, indicating that the brominated pollutant could modulate the development of tumors in vivo (Brito et al, 2020). In addition, the animals from BDE-209 and BDE-209 + dacarbazine groups had more tumors than those from the dacarbazine group.…”

Section: ) Discussionmentioning

confidence: 53%

“…It is well described that both the health of patients and environmental conditions can modulate the development of cancer, but few studies reported the role of pollutants in cancer prognosis or its effects on cancer treatment e cacy. Recently, we reported the modulation of BDE-209 increasing the metastatic spread of melanoma in the lung, brain, liver and gonads of C57BL/6 mice (Brito et. al., 2020).…”

Section: ) Discussionmentioning

confidence: 99%

“…According to Huang et al (2007) and Wang and Huang, (2007), many anticancer drugs, including methotrexate, paclitaxel, uorouracil, capecitabine, gemcitabine and topotecan present sex differences in their clearance. Foremost, BDE-209 showed to favor the metastatic spread of melanoma in the lung of mice (Brito et al, 2020), and impaired the dacarbazine bene cial effects on metastatic melanoma treatment. These ndings highlight the role of BDE-209 on cancer prognosis and the high sensitivity of female mice to dacarbazine treatment and polybrominated exposure, revealing that human lifestyle is vital for cancer treatment e cacy.…”

Section: ) Discussionmentioning

confidence: 99%

“…In the current study, the effects of BDE-209 were investigated in mice exposed to BDE-209, inoculated with B16-F10 murine melanoma cells and then treated with dacarbazine, to address whether BDE-209 can interfere with melanoma treatment and lead to a worse prognosis. The study was based on a recent report that BDE-209 exposure can increase the incidence of melanoma metastases in different organs of mice previously exposed to BDE-209 (Brito et. al., 2020).…”

Section: ) Introductionmentioning

confidence: 99%

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

Manuitt-Brito

Souza

Neto

et al. 2021

Preprint

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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.

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Section: ) Discussionmentioning

confidence: 53%

Section: ) Discussionmentioning

confidence: 99%

Section: ) Discussionmentioning

confidence: 99%

Section: ) Introductionmentioning

confidence: 99%

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

Manuitt-Brito

Souza

Neto

et al. 2021

Preprint

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“…These compounds have been found in foods with high-fat contents, breast milk and even in intrauterine development [18][19][20]. Despite carcinogenic effects being well-described for various chemicals, our group published the first in vivo study correlating POPs with the progression and increased malignancy of an established type of cancer [21]. In the current study, we investigated the role of TCDD and BDE-209 in the modulation of ABC transporter proteins in murine melanoma cells (B16-F1) after acute and chronic exposure at concentrations previously found in human plasma.…”

Section: Introductionmentioning

confidence: 99%

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

Marchi¹,

Moggio²,

Neto³

et al. 2021

IJCST

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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.

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Role of autonomic nervous system in BDE‐209 maternal exposure induced immunotoxicity in female offspring

Mao,

Tang,

et al. 2024

Environmental Toxicology

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Decabrominated diphenyl ether (BDE‐209) is a typical persistent organic pollutant that can cross the placental barrier, increasing the exposure risk for offspring. Norepinephrine (NE) from nerve terminals and acetylcholine (Ach) can bind to specific receptors on immune cells, inhibit the immune function of the body then cause immunotoxicity. However, whether maternal exposure to BDE‐209 could lead to immunotoxicity in the offspring by acting on the sympathetic and parasympathetic nervous systems remains unclear. In view of this, the pregnancy and lactation rat BDE‐209 exposure model was established and the results demonstrated that pregnancy and lactation BDE‐209 exposure could induce immunotoxicity to female offspring via affecting immunopathology (hematological and biochemical parameters, organ indices, and spleen histopathological), decreasing humoral immunity (serum hemolysin, immunoglobulins, and cytokine productions), damaging cellular immunity (splenic lymphocytes and spleen cytokine productions), and restraining nonspecific immunity. Moreover, a dramatically significant correlation was observed between spleen nerve indices and immunity indices. Additionally, the mechanism revealed that maternal BDE‐209 exposure caused offspring immunotoxicity through (1) activating MHC/PKCθ/NF‐κB pathway; (2) promoting sympathetic nervous pathway, by upregulating the expression of β2AR protein, which in turn elevating cAMP, following activate PKA and phosphorylate CREB, ultimately leading to immunotoxicity;(3) activating parasympathetic nerve pathway by reducing the binding with Ach and α7nAchR, upregulating the expression of JAK2 and phosphorylating STAT3, induced immunotoxicity of female offspring.

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

Cited by 12 publications

References 44 publications

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

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

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

Role of autonomic nervous system in BDE‐209 maternal exposure induced immunotoxicity in female offspring

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