Xin Zhao

Co-contamination of biphenyl and heavy metals is widespread in industrial environments, but systematic studies on the simultaneous treatment of both pollutants using a single microbial strategy remain limited. In this study, we characterized the biphenyl degradation performance, metabolic pathway, transcriptomic response, and Cr(VI) tolerance of Rhodococcus sp. TG-1, and developed an alkali-modified biochar immobilization system to enhance its degradation efficiency for biphenyl under Cr(VI) stress. Degradation experiments were carried out under optimal conditions (30 °C, pH 7.0), and it was found that strain TG-1 degraded 76.84% of 300 mg/L biphenyl within 3 days. Intermediate metabolites were identified by LC-MS, and five key intermediates were detected, confirming that TG-1 metabolizes biphenyl via the classical 2,3-dihydroxybiphenyl dioxygenase pathway, with subsequent entry into the tricarboxylic acid cycle. Transcriptomic analysis was performed to profile gene expression, revealing 845 differentially expressed genes under biphenyl stress, including 672 upregulated genes significantly enriched in aromatic degradation pathways. Seven complete bph gene clusters responsible for biphenyl catabolism were also identified. Strain TG-1 exhibited high tolerance to Cr(VI), with a minimum inhibitory concentration (MIC) of 500 mg/L. However, its biphenyl degradation efficiency dropped to 51.32% in the presence of 200 mg/L Cr(VI). After immobilization using alkali-modified straw biochar (JBC), heavy metal toxicity was alleviated, and the biphenyl removal rate increased to 99.30% under co-contamination conditions. Scanning electron microscopy (SEM) and Fourier transform infrared spectroscopy (FTIR) analyses confirmed that TG-1 was stably loaded onto the biochar surface through hydrogen bonding and electrostatic interactions. Altogether, this study provides a promising bacterial strain and a green immobilization strategy for enhancing biphenyl removal in the presence of Cr(VI), offering a practical approach for the treatment of environments co-contaminated with aromatic compounds and heavy metals.

Co-contamination with dibenzofuran (DBF) and cadmium (Cd(II)) poses a major challenge in environmental remediation. While Burkholderia sp. can degrade polycyclic aromatic hydrocarbons and tolerate heavy metals, the coordinated mechanism governing DBF degradation under high Cd(II) stress remains elusive. Here, we characterize Burkholderia sp. FM-2, which optimally degrades 600 mg/L DBF at pH 6.0 and 25 °C, achieving 91.8% removal within 48 h. FM-2 exhibits exceptional Cd(II) tolerance, with a minimum inhibitory concentration of 2000 mg/L. UPLC-MS/MS confirms DBF degradation via dioxygenase-mediated hydroxylation and sequential enzymatic reactions. Transcriptomics reveals, for the first time, concurrent upregulation of genes encoding RND efflux pumps, ABC transporters, P-type ATPases, and core DBF-degrading enzymes under high Cd(II) stress, enabling the synergistic maintenance of intracellular Cd(II) homeostasis and efficient DBF degradation. Collectively, FM-2 remediates DBF-Cd(II) co-contamination via coordinated transcriptional regulation of degradation and detoxification pathways, offering a promising strain resource and molecular basis for the bioremediation of co-contaminated environments.

Against the backdrop of escalating global plastic pollution, there is an urgent need to elucidate the systemic health risks posed by nanoplastics (NPs) as emerging environmental contaminants that enter higher organisms through the food chain. This study employed a three-level trophic transfer model, examining the pathway from polystyrene nanoparticles to Tenebrio molitor larvae and subsequently to mice, offering a comprehensive elucidation of the mechanisms behind the multiorgan toxicity associated with food chain-transferred nanoplastics (FCT-NPs). Our results demonstrated extensive accumulation of FCT-NPs across multiple organs via systemic circulation. Integrative multiorgan omics analysis revealed that FCT-NPs primarily induced two major categories of multiorgan comorbidities: cardiovascular diseases and metabolic disorders, with the liver identified as a central metabolic hub that potentially regulates other organs through bile acid-mediated metabolic crosstalk. Mechanistically, dysregulation of key genes, such as MTOR and FN1, activated Wnt and TGF-β signaling pathways, which in turn promoted organ fibrosis. Additionally, aberrant expression of critical regulators─including CAT, LPL, NQO1, and APOE─was found to drive oxidative stress and disrupt lipid metabolism. These findings provide crucial scientific evidence for FCT-NPs risk assessment and underscore the imperative for enhanced plastic pollution control and further investigation into long-term exposure effects.