Pesticide chlorothalonil is widely applied in tea agroecosystem, potentially disturbing soil microbial-mediated nitrogen cycle. The underlying toxicity mechanism, however, is not well explored. Here, we investigated the long-term effects of chlorothalonil on soil microbial denitrification and N2O emission pattern in a tea field after 40 days of exposure. Results showed that chlorothalonil inhibited denitrification process but remarkably promoted N2O emission by 380-830%. Chlorothalonil significantly inhibited N2O reductase activity but did not affected nosZ abundance. Our results further revealed that chlorothalonil influenced soil denitrification by directly suppressing microbial electron transport system activity, and decreasing electron donor nicotinamide adenine dinucleotide (NADH) and energy source adenosine triphosphate (ATP) levels. Additionally, chlorothalonil also downregulated denitrifying functional genes (narG, nirS, and norB) and declined the relative abundances of potential denitrifiers (i.e., Pseudomonas and Streptomyces). Stepwise regression and path modeling suggested that nitrate reductase was the most significant factor in explaining denitrification rate under chlorothalonil applications. This study provides important information for revealing the chronic impacts of pesticide on tea soil denitrification and N2O emission on the basis of electron transport mechanism. Most significantly, N2O emission is underestimated in chlorothalonil-treated soils, which suggests that future estimations of N2O emission from agricultural lands should take account of pesticide dependency conditions.
Keywords: Denitrification; Enzyme activity; Microbial community; N2O emission; Pesticide.