Microbial degradation is considered the most promising method for removing phthalate acid esters (PAEs) from polluted environments; however, a comprehensive genomic understanding of the entire PAE catabolic process is still lacking. In this study, the repertoire of PAE catabolism genes in the metabolically versatile bacterium Rhodococcus sp. 2G was examined using genomic, metabolic, and bioinformatic analyses. A total of 4930 coding genes were identified from the 5.6 Mb genome of the 2G strain, including 337 esterase/hydrolase genes and 48 transferase and decarboxylase genes that were involved in hydrolysing PAEs into phthalate acid (PA) and decarboxylating PA into benzoic acid (BA). One gene cluster (xyl) responsible for transforming BA into catechol and two catechol-catabolism gene clusters controlling the ortho (cat) and meta (xyl &mhp) cleavage pathways were also identified. The proposed PAE catabolism pathway and some key degradation genes were validated by intermediate-utilising tests and real-time quantitative polymerase chain reaction. Our results provide novel insight into the mechanisms of PAE biodegradation at the molecular level and useful information on gene resources for future studies.
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http://dx.doi.org/10.1016/j.scitotenv.2018.05.337 | DOI Listing |
Cancer Manag Res
January 2025
Lung Cancer Center, West China Hospital, Sichuan University, Chengdu, People's Republic of China.
Objective: Our research has pinpointed the gut microbiome's role in the progression of various pathological types of non-small cell lung cancer (NSCLC). Nonetheless, the characteristics of the gut microbiome and its metabolites across different clinical stages of NSCLC are yet to be fully understood. The current study seeks to explore the distinctive gut flora and metabolite profiles of NSCLC patients across varying TNM stages.
View Article and Find Full Text PDFBackground: The increased use of chemicals leads to a continuous deposition of chemicals in the environment and to a continuous increase in exposure of the global and the European population. Comprehensive burden of disease analyses are however still missing for many countries.
Methods: Using the World Health Organization's Environmental Burden of Disease (EBD) approach and combining data from the European Human Biomonitoring (HBM) dashboard with disease and population data, we estimated the comprehensive attributable burden (AB) for the year 2021, in the best-case quantified by disability-adjusted life years (DALY).
Reprod Toxicol
January 2025
Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville 3010, Australia; Murdoch Children's Research Institute, Royal Children's Hospital, Parkville 3010, Australia; Department of Paediatrics, University of Melbourne, Parkville 3010, Australia. Electronic address:
Phthalates are ubiquitous environmental pollutants known for their endocrine-disrupting properties, particularly during critical periods such as pregnancy and early childhood. Phthalates alter lipid metabolism, but the role of prenatal exposure on the offspring lipidome is less understood. In particular, we focused on long chain acylcarnitines - intermediates of fatty acid oxidation that serve as potential biomarkers of mitochondrial function and energy metabolism.
View Article and Find Full Text PDFJ Hazard Mater
January 2025
State Key Laboratory of Environmental Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing 100012, China. Electronic address:
The remediation of sites co-contaminated with polycyclic aromatic hydrocarbons (PAHs) and heavy metals (HMs) poses challenges for efficient and ecofriendly restoration methods. In this study, three strains (Pseudomonas sp. PDC-1, Rhodococcus sp.
View Article and Find Full Text PDFFood Chem Toxicol
January 2025
RECETOX, Faculty of Science, Masaryk University, Kotlářská 2, 61137 Brno, Czech Republic. Electronic address:
Endocrine-disrupting compounds (EDCs) may contribute to the rising incidence of metabolic dysfunction-associated steatotic liver disease (MASLD). We investigated the potential of 10 environmentally relevant EDCs to affect key events of hepatic steatosis in HepG2 human hepatoma cells. Increased lipid droplet formation, a key marker of steatosis, was induced by PFOA, bisphenol F, DDE, butylparaben, and DEHP, within the non-cytotoxic concentration range of 1 nM-25 μM.
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