Biodegradation of petroleum hydrocarbons based pollutants in contaminated soil by exogenous effective microorganisms and indigenous microbiome.

Microbial remediation is an eco-friendly and promising approach for the restoration of sites contaminated by petroleum hydrocarbons (PHCs). The degradation of total petroleum hydrocarbons (TPHs), semi volatile organic compounds (SVOCs) and volatile organic compounds (VOCs) of the soil samples collected from a petrochemical site by indigenous microbiome and exogenous microbes (Saccharomyces cerevisiae ATCC 204508/S288c, Candida utilis AS2.281, Rhodotorula benthica CBS9124, Lactobacillus plantarum S1L6, Bacillus thuringiensis GDMCC1.817) was evaluated. Community structure and function of soil microbiome and the mechanism involved in degradation were also revealed. After bioremediation for two weeks, the concentration of TPHs in soil samples was reduced from 17,800 to 13,100 mg/kg. The biodegradation efficiencies of naphthalene, benzo[a]anthracene, benzo[b]fluoranthene, benzo[a]pyrene, indeno[1,2,3-cd]pyrene, dibenzo[a,h]anthracene, 1,2,3-trichloropropane, 1,2-dichloropropane, ethylbenzene and benzene in soil samples with the addition of S. cerevisiae were 38.0%, 35.7%, 36.2%, 40.4%, 33.6%, 36.2%, 12.0%, 43.9%, 43.3% and 43.0%, respectively. The microbial diversity and community structure were improved during the biodegradation process. S. cerevisiae supplemented soil samples exhibited the highest relative abundance of the genus Acinetobacter for bacteria and Saccharomyces for yeast. The findings offer insight into the correlation between microbes and the degradation of PHC-based pollutants during the bioremediation process.

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.

Proteome and phospholipid alteration reveal metabolic network of Bacillus thuringiensis under triclosan stress.

Triclosan is a common antibacterial agent widely applied in various household and personal care products. The molecule, cell, organ and organism-level understanding of its toxicity pose to some target organisms has been investigated, whereas, the alteration of a single metabolic reaction, gene or protein cannot reflect the impact of triclosan on metabolic network. To clarify the interaction between triclosan stress and metabolism at network and system levels, phospholipid synthesis, and cellular proteome and metabolism of Bacillus thuringiensis under 1µM of triclosan stress were investigated through omics approaches. The results showed that C14:0, C16:1ω7, C16:0 and C18:2ω6 were significantly up-produced, and 19 proteins were differentially expressed. Whereas, energy supply, protein repair and the synthesis of DNA, RNA and protein were down-regulated. PyrH and Eno could be biomarkers to reflect triclosan stress. At network level, the target proteins ACOX1, AHR, CAR, CYP1A, CYP1B1, DNMT1, ENO, HSP60, HSP70, SLC5A5, TPO and UGT expressed in different species shared high sequence homology with the same function proteins found in Homo sapiens not only validated their role as biomarkers but also implied the potential impact of triclosan on the metabolic pathways and network of humans. These findings provided novel insights into the metabolic influence of triclosan at network levels, and developed an omics approach to evaluate the safety of target compound.

UV-driven hydroxyl radical oxidation of tris(2-chloroethyl) phosphate: Intermediate products and residual toxicity.

Organophosphorus esters (OPEs) are emerging contaminants widely applied as annexing agents in a variety of industrial products, and they are robust against conventional wastewater treatments. Ultraviolet-driven (UV) radical-based advanced oxidation processes have a potential to become cost-effective treatment technologies for the removal of OPEs in water matrix, but residual and newly generated toxicities of degradation products are a concern. This study is a comprehensive attempt to evaluate UV/H2O2 for the degradation of a water dissolved OPE, tris(2-chloroethyl) phosphate (TCEP). In ultrapure water, a pseudo-first order reaction was observed, and the degradation rate constant reached 0.155 min-1 for 3.5 µM TCEP using 7.0 mW cm-2 UV irradiation with 44.0 µM H2O2. Hydroxyl radicals were involved in the oxidative degradation of TCEP, as demonstrated by the quenching of the degradation reaction in the presences of tertiary butanol or ethanol. High resolution mass spectroscopy data showed a partial transformation of TCEP to a series of hydroxylated and dechlorinated products e.g., C4H9Cl2O4P, C6H13Cl2O5P and C2H6ClO4P. Based on proteomics data at molecular and metabolic network levels, the toxicity of TCEP products was reduced obviously as the reaction proceeded, which was confirmed by the up-regulated tricarboxylic acid cycle, fatty acid metabolism and amino acid metabolism in Escherichia coli cells exposed to degradation products mixture. In conclusion, incomplete hydroxylation and dechlorination of TCEP likewise are effective for its detoxification, indicating that UV/H2O2 can be a promising treatment method for OPEs removal.

Heterogeneous photocatalysis of tris(2-chloroethyl) phosphate by UV/TiO2: Degradation products and impacts on bacterial proteome.

The widespread, persistent and toxic organophosphorus esters (OPEs) have become one category of emerging environmental contaminants. Thus, it is in urgent need to develop a cost-effective and safe treatment technology for OPEs control. The current study is a comprehensive attempt to use UV/TiO2 heterogeneous photocatalysis for the degradation of a water dissolved OPEs, tris(2-chloroethyl) phosphate (TCEP). A pseudo-first order degradation reaction with a kobs of 0.3167 min-1 was observed, while hydroxyl radical may be the dominating reactive oxidative species. As the reaction proceeded, TCEP was transformed to a series of hydroxylated and dechlorinated products. The degradation efficiency was significantly affected by pH value, natural organic matters and anions, implying that the complete mineralization of TCEP would be difficult to achieve in actual water treatment process. Based on the proteomics analysis regarding the metabolism reactions, pathways and networks, the significant activation of transmembrane transport and energy generation in Escherichia coli exposed to preliminary degrading products suggested that they can be transported and utilized through cellular metabolism. Furthermore, the descending trend of stress resistance exhibited that the toxicity of products was obviously weakened as the treatment proceeded. In conclusion, hydroxylation and dechlorination of TCEP with incomplete mineralization were likewise effective for its detoxification, indicating that UV/TiO2 will be an alternative treatment method for OPEs control.