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

Benzo[a]pyrene (B[a]P) and polybrominated diphenyl ethers (PBDEs) are persistent environmental contaminants. The effects in organisms of exposures to binary mixtures of such contaminants remain obscure. Attenuated total reflection Fourier-transform infrared (ATR-FTIR) spectroscopy is a label-free, non-destructive analytical technique allowing spectrochemical analysis of macromolecular components, and alterations thereof, within tissue samples. Herein, we employed ATR-FTIR spectroscopy to identify biomolecular changes in rat liver post-exposure to B[a]P and BDE-47 (2,2',4,4'-tetrabromodiphenyl ether) congener mixtures. Our results demonstrate that significant separation occurs between spectra of tissue samples derived from control versus exposure categories (accuracy = 87%; sensitivity = 95%; specificity = 79%). Additionally, there is significant spectral separation between exposed categories (accuracy = 91%; sensitivity = 98%; specificity = 90%). Segregation between control and all exposure categories were primarily associated with wavenumbers ranging from 1600 to 1700 cm-1 . B[a]P and BDE-47 alone, or in combination, induces liver damage in female rats. However, it is suggested that binary exposure apparently attenuates the toxic effects in rat liver of the individual contaminants. This is supported by morphological observations of liver tissue architecture on hematoxylin and eosin (H&E)-stained liver sections. Such observations highlight the difficulties in predicting the endpoint effects in target tissues of exposures to mixtures of environmental contaminants.

Whole transcriptome sequencing and competitive endogenous RNA regulation network construction analysis in benzo[a]pyrene-treated breast cancer cells.

Breast cancer is the most common malignant tumor in women worldwide, and environmental pollutants are considered to be risk factors. Currently, most studies into benzo[a]pyrene (B[a]P)-induced breast cancer focus on biological effects such as proliferation, invasion, and metastasis, DNA damage, estrogen receptor (ER)-related molecular mechanisms, oxidative damage, and other metabolic pathways. This study aims to provide insights into the role of B[a]P in breast cancer development through RNA-seq and bioinformatics analysis and construction of a competing endogenous RNA (ceRNA) regulatory network. By analyzing RNA-seq results, we identified 144 differentially-expressed circRNAs, 69 differentially-expressed lncRNAs, 20 differentially-expressed miRNAs, and 212 differentially-expressed mRNAs. Following on, we analyzed the gene ontology (GO) and KEGG enrichment functions of the differentially-expressed RNAs. In addition, the protein-protein interaction (PPI) network was mapped for differentially-expressed mRNAs. Subsequently, we constructed ceRNA networks, one of which consisted of 45 dysregulated circRNAs, 11 miRNAs, and 9 mRNAs, and a second consisted of 40 lncRNAs, 11 miRNAs, and 9 mRNAs. Finally, 6 circRNAs, 4 lncRNAs, 1 miRNA, and 4 mRNAs were randomly selected for quantitative real-time PCR verification. PCR results were further verified by Western blotting assays. These results show that the expression level of differentially-expressed RNA was consistent with the sequencing data, and the Western blotting results were highly consistent with the PCR results, confirming that the sequencing result was very reliable. This study systematically explores the ceRNA atlas of differentially-expressed genes related to B[a]P exposure in breast cancer cells, providing new insights into mechanisms of environmental pollutants in breast cancer.