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Molecular mechanism of diclofenac sodium on the toxicity of Bacillus thuringiensis |
WU Shuang, QIN Hua-ming, YE Jin-shao |
Key Laboratory of Environmental Exposure and Health of Guangzhou, Guangdong Provincial Research Center for Environment Pollution Control and Remediation Materials, School of Environment, Jinan University, Guangzhou 510632, China |
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Abstract To investigate the molecular toxicity of diclofenac sodium to Bacillus thuringiensis, the iTRAQ quantitative proteomics technique was used to identify and quantify the protein expression of this species. The results showed that diclofenac sodium had a significant inhibitory effect on the growth of B. thuringiensis. Seventeen proteins were differentially expressed. Among these proteins, 5up-regulated ones were mainly involved in fatty acid biosynthesis, DNA and RNA synthesis, while 12down-regulated proteins were primarily associated with oxidative phosphorylation, pyruvate metabolism, glycolytic pathway, pentose phosphate pathway and amino acid metabolism. Functional analysis revealed that diclofenac inhibited the growth of B. thuringiensis by affecting cell metabolism, cellular composition and protein catalysis. In the interaction network of differentially expressed proteins, RpoA, RplM, RplL, Tuf, InfA were the key nodes in the network interacting closely for cellular regulation. The results indicated that diclofenac sodium could affect multiple metabolic pathways and interfere with different biological processes. These findings revealed the molecular toxicity of diclofenac sodium, and provided important references for the further evaluation of diclofenac sodium on the ecological security and human health.
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Received: 18 May 2017
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