4.7 Article

Different utilizable substrates have different effects on cometabolic fate of imidacloprid in Stenotrophomonas maltophilia

Journal

APPLIED MICROBIOLOGY AND BIOTECHNOLOGY
Volume 97, Issue 14, Pages 6537-6547

Publisher

SPRINGER
DOI: 10.1007/s00253-012-4444-y

Keywords

Imidacloprid; Biocometabolism; Utilizable substrate; Cofactor

Funding

  1. Priority Academic Program Development of Jiangsu Higher Education Institutions
  2. Key Basic Research Program of Jiangsu Higher Education Institution of China [06KJA21016]
  3. National Science Foundation of China [30970040]
  4. Program of Jiangsu Higher Education Institution of China [09KJB180003]

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Imidacloprid, the largest selling insecticide in the world, is more stable in soil, and its environmental residue and effects are attracting people's close attention. One of imidacloprid metabolism pathways was degraded to CO2 through olefin imidacloprid pathway. Here, we report that sucrose as a utilizable substrate enhanced the cometabolism of imidacloprid by Stenotrophomonas maltophilia CGMCC 1.1788 to produce 5-hydroxy imidacloprid, whereas when succinate was used as a utilizable substrate, 5-hydroxy imidacloprid from imidacloprid was transformed to olefin imidacloprid, and the latter was further degraded. The hydroxylation of imidacloprid required NAD(P)H, whereas the dehydration of 5-hydroxy imidacloprid to form olefin imidacloprid required succinate rather than NAD(P)H. NADPH greatly favored the hydroxylation of imidacloprid more than NADH, and NADPH inhibited the dehydration of 5-hydroxy imidacloprid to olefin imidacloprid, but NADH did not. Therefore, sucrose may be metabolized through hexose monophosphate pathway to produce mainly NADPH which participated in the hydroxylation of imidacloprid to 5-hydroxy imidacloprid and meanwhile inhibited the dehydration of 5-hydroxy imidacloprid to olefin imidacloprid, whereas succinate may be metabolized mainly through the tricarboxylic acid cycle to produce NADH which was involved in hydroxylation of imidacloprid to 5-hydroxy imidacloprid but did not inhibit the dehydration of 5-hydroxy imidacloprid to olefin imidacloprid. Our results have a significant meaning in further understanding the influence of different utilizable substrates on the cometabolic pathways and the fate of environmental imidacloprid.

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