Modulation of Benzo[a]pyrene-Induced Toxic Effects in Japanese Medaka (Oryzias latipes) by 2,2′,4,4′-Tetrabromodiphenyl Ether

Abstract

Because polycyclic aromatic hydrocarbons (PAHs) and polybrominated diphenylethers (PBDEs) are ubiquitous and coexist in the environment and in wildlife, there are potential interactions between them that could cause toxic effects. In this study, the modulating effects of 2,2',4,4'-tetrabromodiphenyl ether (BDE47) and benzo[a]pyrene (BaP)-induced reproductive and developmental toxic effects in Japanese medaka (Oryzias latipes) were investigated by exposing adult Japanese medaka to BaP alone, BDE47 alone, and coexposing them with both BaP and BDE47 at different concentrations, respectively. Exposure to BaP alone significantly suppressed fecundity and egg protein content and markedly induced skeletal deformation in F1 generation eleutheroembryos. BDE47 significantly recovered reproductive functions, fecundity, and egg protein content, suppressed by BaP when the concentration of BDE47 increased to 0.44 μg/L. Such effects can be at least partly explained by the decreased BaP levels in the coexposure groups and the accompanying increase in the circulating level of 17β-estradiol in female medaka fish. The prevalence of skeletal deformations markedly increased to 19.3 ± 2.4% and 16.0 ± 1.6% in fish coexposed to BaP and BDE47 at 0.44 and 2.58 μg/L compared with that of fish exposed to 1.21 μg/L BaP alone (9.7 ± 1.7%), and the impacts on male medaka fish in the coexposure groups would be the crucial reason leading to these effects. Considering that the measured water concentrations of BaP and BDE47 in the present study were comparable with those reported in rivers and harbors, BaP and BDE47 contamination in the real world would have a significant level of interactive effects on wild fish.

Effects of co-exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin and polychlorinated biphenyls on nonalcoholic fatty liver disease in mice

“…Owing to their highly lipophilic nature, slow metabolism, and high toxicity (Miniero et al, ; Sorg et al, ), they have a long half life in the body and cause many diseases such as hypertension, diabetes, metabolic syndrome, and atherosclerosis. Because humans are ubiquitously and simultaneously exposed to mixtures of these persistent organic pollutants (POPs) (Zhao et al, ), it is important to assess the mixture effects of multiple pollutants.…”

Families of Nuclear Receptors in Vertebrate Models: Characteristic and Comparative Toxicological Perspective

“…For example, ERs, AR and THRs, involved in development and maintenance of the endocrine system, have been demonstrated to be targets of alkylphenols, phthalates (PAEs), dichlorodiphenyltrichloroethane and some metabolites of polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDE) 11 12 13 . Besides endocrine receptors, PXR and CAR, NRs that participate in metabolism of both endobiotics and xenobiotics to detoxify or bioactivate chemicals, can be activated by a variety of pharmaceuticals such as rifampicin, pesticides such as chlorpyrifos and methoxychlor, and other synthetic chemicals used in industry, such as PBDEs and BPA 14 15 16 17 In addition to these well-known NRs, there are more NRs, that, during the past decade, have been identified in genomes of several vertebrates. These include 48 NR genes in human ( Homo sapiens ), 47 genes in rat ( Rattus norvegicus ), 49 genes in mouse ( Mus musculus ) and 68 genes in the teleost puffer fish Fugu rubripes 18 19 .…”

Spectrochemical determination of effects on rat liver of binary exposure to benzo[a]pyrene and 2,2′,4,4′‐tetrabromodiphenyl ether

“…Although the microscopic examination of H&E‐stained slides suggests that the binary‐exposure category appears counter‐intuitively to exhibit a reduced level of liver injury compared with the single exposure categories, this would need to be confirmed in parallel standard toxicity assays looking at transcriptomic/protein alterations (e.g., CYP isoforms), enzyme leakage, energy status and genomic damage. To speculate on underlying mechanism, it has been found that the presence of BDE‐47 significantly reduces the toxic effects of B[ a ]P in Oryzias latipes larvae (Zhao et al, 2013). To this end, it has been noted that exposure to B[ a ]P can induce up‐regulation of CYP1A gene expression (Zhang et al, 2015).…”

“…CYP1A can metabolize organic pollutants into active intermediates, thus producing toxic effects. However, BDE‐47 exposure may significantly inhibit the expression of CYP1A , thus reducing the toxic effects of B[ a ]P (Zhao et al, 2013). The attenuation of B[ a ]P‐induced CYP1A expression by BDE‐47 was also observed in a previous in vitro test, in which L02 cells pre‐treated with BDE‐47 could significantly decrease B[ a ]P‐induced CYP1A expression (An et al, 2011).…”