Zuqiang Cao,Juan Chen,Chao Wang,Peifang Wang,Han Gao,Bingbing Feng,Bo Zhang,Rong Wang,Ge Cui
Periphytic biofilms are ubiquitous and drive biogeochemical nutrient cycling in paddy ecosystems. However, the mechanisms of multi-kingdom microbial interactions regulating nitrogen (N) cycling in the biofilms remain unexplored. This study conducted a microcosm experiment to investigate the effects of imidacloprid (IMI), a widely used neonicotinoid pesticide, on N cycling in periphytic biofilms. Throughout the 30-day experiment, 0.02–0.12 mg of N was lost from the water-biofilm microcosm systems, increasing with higher IMI exposure concentrations. Metatranscriptomic sequencing demonstrated 84.3 %–92.2 % downregulation of nitrification genes and 33.9 %–143 % upregulation of denitrification genes in the biofilms. These alterations in gene expression were regulated by microbial competition and cooperation within ecological clusters associated with the biofilm potential nitrification and denitrification activities, respectively. Correlation between the relative abundance of microorganisms in these clusters and gene abundance revealed multi-kingdom nitrifying and denitrifying communities, including Nitrosopumilus (Archaea) and Nitrospira (Bacteria) for nitrification, and Enterococcus (Bacteria) and Aspergillus (Fungi) for denitrification. Partial least squares path modeling indicated that the biofilm-mediated N loss was driven by promoted denitrification (total effect = −0.83) rather than suppressed nitrification (total effect = 0.52). Our findings highlight multi-kingdom microbial interactions regulating N cycling in periphytic biofilms and neonicotinoid pesticide risks.
Epidemiological evidence on the health effects of pesticide exposure among greenhouse workers is limited, and the mechanisms are lacking. Building upon our team’s previous population study, we selected two pesticides, CPF and EB, with high detection rates, based on the theoretical foundation that the liver serves as a detoxifying organ, we constructed a toxicity model using HepG2 cells to investigate the impact of individual or combined pesticide exposure on the hepatic metabolism profile, attempting to identify targeted biomarkers. Our results showed that CPF and EB could significantly affect the survival rate of HepG2 cells and disrupt their metabolic profile. There were 117 metabolites interfered by CPF exposure, which mainly affected ABC transporter, biosynthesis of amino acids, center carbon metabolism in cancer, fatty acid biosynthesis and other pathways, 95 metabolites interfered by EB exposure, which mainly affected center carbon metabolism in cancer, HIF-1 signaling pathway, valine, leucine and isoleucine biosynthesis, fatty acid biosynthesis and other pathways. The cross analysis and further biological experiments confirmed that CPF and EB pesticide exposure may affect the HIF-1 signaling pathway and valine, leucine and isoleucine biosynthesis in HepG2 cells, providing reliable experimental evidence for the prevention and treatment of liver damage in greenhouse workers.
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