Metabolic and proteomic mechanism of bisphenol A degradation by Bacillus thuringiensis.

Bisphenol A (BPA) is a worldwide, widespread pollutant with estrogen mimicking and hormone-like properties. To date, some target biomolecules associated with BPA toxicity have been confirmed. The limited information has not clarified the related metabolism at the pathway and network levels. To this end, metabolic and proteomic approaches were performed to reveal the synthesis of phospholipids and proteins and the metabolic network during the BPA degradation process. The results showed that the degradation efficiency of 1 μM of BPA by 1 g L-1 of Bacillus thuringiensis was up to 85% after 24 h. During this process, BPA significantly changed the membrane permeability; altered sporulation, amino acid and protein expression, and carbon, purine, pyrimidine and fatty acid metabolism; enhanced C14:0, C16:1ω7, C18:2ω6, C18:1ω9t and C18:0 synthesis; and increased the trans/cis ratio of C18:1ω9t/C18:1ω9c. It also depressed the spore DNA stability of B. thuringiensis. Among the 14 upregulated and 7 down-regulated proteins, SasP-1 could be a biomarker to reflect BPA-triggered spore DNA impairment. TpiA, RpoA, GlnA and InfA could be phosphorylated at the active sites of serine and tyrosine. The findings presented novel insights into the interaction among BPA stress, BPA degradation, phospholipid synthesis and protein expression at the network and phylogenetic levels.