The problem of soil polycyclic aromatic hydrocarbon (PAH) pollution in coking plant sites has been widely studied in recent years, but there is a lack of research on the correlation between soil microorganisms, soil metabolomics, and soil properties. Thus, in this study, the long-term impact of coke combustion on soil microbial community structure, enzyme activities, and metabolic pathways within a former coking plant site was investigated. Soil samples were collected from both the coking production area (CA group) and office area (OLA group), approximately 0 to 20 cm in depth. Compared with OLA group, elevated levels of 16 PAHs in the list of US EPA were detected by gas chromatography-mass spectrometry in the CA group. Several dominant microorganisms, such as Altererythrobacter, Lysobacter, and Sulfurifustis, were identified by 16 s ribosomal DNA sequencing in the CA group. The fatty acid biosynthesis pathway exhibited specific inhibition, while the phenylalanine metabolic pathway was promoted in response to PAH stress. Long-term PAH exposure led to the inhibition of soil urease activity. The co-occurrence network of microorganisms revealed intricate patterns of co-metabolism and co-adaptation within complex bacterial communities, facilitating their adaptation to and decomposition of soil-borne PAHs. This research could provide valuable insights into the community characteristics and metabolic mechanisms of microorganisms inhabiting PAH-polluted soil within coking plant sites. The findings enhance our understanding of the indigenous soil microbiome and its intricate network dynamics under the persistent stress of PAHs, contributing to a more comprehensive knowledge of soil ecosystems in such environments.

The evaluation of toxicity related to polychlorinated dibenzo-p-dioxins and furans (PCDD/Fs) and dioxin-like polychlorinated biphenyls (DL-PCBs) is crucial for a comprehensive risk assessment in real-world exposure scenarios. This study employed a controlled feeding experiment to investigate the metabolic effects of dioxin-like compounds (DLCs) on laying hens via feed exposure. Diets enriched with two concentrations (1.17 and 5.13 pg toxic equivalents (TEQ) /g dry weight (dw)) were administered over 14 days, followed by 28 days of clean feed. Metabolomics analyses of blood samples revealed significant metabolic variations between PCDD/Fs and DL-PCBs exposed groups and controls, reflecting the induced metabolic disruption. Distinct changes were observed in sphingosine, palmitoleic acid, linoleate, linolenic acid, taurocholic acid, indole acrylic acid, and dibutyl phthalate levels, implying possible connections between PCDD/Fs and DL-PCBs toxic effects and energy-neuronal imbalances, along with lipid accumulation and anomalous amino acid metabolism, impacting taurine metabolism. Moreover, we identified three differential endogenous metabolites—L-tryptophan, indole-3-acetaldehyde, and indole acrylic acid—as potential ligands for the aryl hydrocarbon receptor (AhR), suggesting their role in mediating PCDD/Fs and DL-PCBs toxicity. This comprehensive investigation provides novel insights into the metabolic alterations induced by PCDD/Fs and DL-PCBs in laying hens, thereby enhancing our ability to assess risks associated with their exposure in human populations.

BACKGROUND:Chlorinated flame retardant Dechlorane 602 (Dec 602) has been detected in daily food, indicating that it may pose a risk to intestinal health. The intestinal microenvironment plays an important role in intestinal health. Intestinal microbiota and metabolites are two important factors for maintaining the microenvironment. However, little is known about the effects of Dec 602 on intestinal microbiota and metabolites.OBJECTIVES:We aimed to probe the effects of Dec 602 on the intestine by revealing the changes that Dec 602 caused to the intestinal microbiota and metabolites.METHODS:Adult female C57BL/6 mice were exposed to Dec 602 (low/high doses: 1.0/10.0 μg/kg body weight per day) orally for 7 consecutive days, and sacrificed after 7 days of recovery. The composition of colonic microbiota was measured by 16S rRNA gene sequencing, and the colonic metabolites were determined by LC-ESI-MS/MS. Finally, the effects of Dec 602 on the colon were validated by histopathological analysis.RESULTS:The intestinal microbiota composition was altered toward a pro-inflammatory status after exposure to Dec 602. Dec 602 exposure also up-regulated oxidative metabolites (glutathione disulfide, taurine and retinoic acid) and pro-inflammatory metabolites (prostaglandin E2). On the other hand, antioxidative metabolites (s-adenosylmethionine and 11-cis-retinol) and anti-inflammatory metabolites (alpha-linolenic acid, eicosapentaenoic acid and docosahexaenoic acid) were down-regulated after exposure to Dec 602. Infiltration of lymphocytes in the colonic lamina propria was observed in the mice treated with Dec 602 for 7 days, and it was not recovered after another 7 days without further treatment.CONCLUSION:Dec 602 interfered with the colonic microbiota and metabolome, and exhibited inflammatory features. Histopathological studies confirmed that Dec 602 exposure did induce colonic inflammation.

Dioxins and dioxin-like compounds (DLCs) in foodstuffs are closely related to human health. As China is the largest food-consuming country, there is a potentially large demand for screening bioassays that are rapid, cost-effective and capable of determining dioxins and DLCs in foodstuffs. CBG2.8D is a reporter gene-based recombinant cell sensor that was recently developed for determining dioxin and DLCs in ambient and seafood samples. In this study, we established a bioanalytical method with this ready-to-use cell sensor for the bioanalysis of dioxins and DLCs in different types of meat samples. Twenty-nine samples from three typical types of meat (beef, pork and fish) were collected and subjected to both instrumental analysis and a CBG2.8D bioassay. The intra- and inter-lab reproducibility of the bioassay was investigated and the coefficients of variation (CVs) were lower than 25%, suggesting that the cell sensor had a good reproducibility for the meat samples. Based on the correlation equation and coefficient obtained by comparing the data from the instrumental analysis and CBG2.8D bioassay, we found that this method had better performance with pork and fish than with beef. The compliance rate was also determined by comparing the results from the instrumental analysis and there were no false results for the pork and fish samples. Lastly, a complete operation procedure was summarized as a guideline for practical application. In conclusion, the CBG2.8D cell sensor exhibits excellent stability and is capable of screening dioxins and DLCs in meat samples.

The homeostasis of gut immunity and microbiota are associated with the health of the gut. Dechlorane 602 (Dec 602) with food web magnification potential has been detected in daily food. People who were orally exposed to Dec 602 may encounter increased risk of health problems in the gut. In order to reveal the influence of short-term exposure of Dec 602 on gut immunity and microbiota, adult female C57BL/6 mice were administered orally with Dec 602 (low/high doses: 1.0/10.0 μg/kg body weight per day) for 7 days. Lymphocytes were examined by flow cytometry. Gut microbiota was measured by 16S rRNA gene sequencing. Results showed that fecal IgA was upregulated after exposure to the high dose of Dec 602, suggesting that there might be inflammation in the gut. Then, changes of immune cells in mesenteric lymph nodes and colonic lamina propria were examined. We found that exposure to the high dose of Dec 602 decreased the percentages of the anti-inflammatory T regulatory cells in mesenteric lymph nodes. In colonic lamina propria, the production of gut protective cytokine interleukin-22 by CD4+ T cells was decreased, and a decreased trend of interleukin-22 production was also observed in type 3 innate lymphoid cells in the high dose group. Furthermore, an altered microbiota composition toward inflammation in the gut was observed after exposure to Dec 602. Additionally, the altered microbiota correlated with changes of immune parameters, suggesting that there were interactions between influenced microbiota and immune parameters after exposure to Dec 602. Taken together, short-term exposure to Dec 602 induced gut immunity and microbiota perturbations, and this might be the mechanisms for Dec 602 to elicit inflammation in the gut.

Emerging evidence supports that exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) impacts the gut microbiota and metabolic pathways. TCDD can be transmitted from mother to child; thus, we hypothesize that maternal exposure to TCDD may affect the gut microbiota in mothers and offspring. To acquire in vivo evidence supporting this hypothesis, female C57BL/6 mice were administered with TCDD (0.1 and 10 μg/kg body weight (bw)) during pregnancy and lactation periods, and then changes of colonic microbiota in offspring and mothers were evaluated. High-throughput sequencing of the V4 regions of the 16S rRNA gene was performed. The composition and structure of the colonic microbiota in offspring and mothers were significantly influenced by 10 μg/kg bw TCDD as demonstrated by upregulation of harmful bacteria and downregulation of beneficial bacteria. Paradoxically, pathogenic bacteria and opportunistic pathogens were conversely decreased in the offspring of the low-dose TCDD treatment group. Tryptophan (Trp) metabolism exhibited a noticeable change caused by the alteration of colonic microbiota in offspring after maternal exposure to 10 μg/kg bw TCDD, which showed a linear dependence, demonstrating that pathogens or opportunistic pathogens may accelerate the dysbiosis of Trp metabolism. Trp metabolism dysregulation caused by the changed colonic microbiota may subsequently impact other intestinal segments or even living organisms. Our study provides new evidence indicating a potential influence of early TCDD exposure on the colonic microbiota and metabolism.

1,3,6,8-Tetrabromocarbazole (1368-BCZ) is identified as an emerging contaminant that exerts angiogenic effects. Multiple studies indicated there was a positive correlation between angiogenesis and nuclear factor kappa B (NF-κB) activation. While the role of NF-κB in inflammation and apoptosis has been well known, the potential biological effects of 1368-BCZ on NF-κB signaling and related mechanism remain unclear. We, therefore, explored the possible effects of 1368-BCZ on the NF-κB pathway at the gene and protein levels and confirmed that NF-κB activation by 1368-BCZ exposure caused an augmented phosphorylated protein level, induction of NF-κB response element (κBRE)-driven luciferase activity and upregulation of transcriptional level of downstream responsive genes. Although 1368-BCZ did not produce detectable changes in hepatic fibrosis in vivo, it obviously altered the apoptosis in human hepatocellular carcinoma (HepG2) cells. Furthermore, the induction of apoptosis was confirmed by the increased cleaved caspase-3 level. These data revealed the activating effects of 1368-BCZ on NF-κB and its involvement in the underlying mechanisms, providing additional information for toxicology studies of emerging contaminants and introducing a mechanism-based toxicological evaluation of emerging pollutants.