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Toxicity and biodegradation of ibuprofen by Bacillus thuringiensis B1(2015b)

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ABSTRACT

In recent years, the increased intake of ibuprofen has resulted in the presence of the drug in the environment. This work presents results of a study on degradation of ibuprofen at 25 mg L−1 in the presence of glucose, as an additional carbon source by Bacillus thuringiensis B1(2015b). In the cometabolic system, the maximum specific growth rate of the bacterial strain was 0.07 ± 0.01 mg mL−1 h−1 and Ksμ 0.27 ± 0.15 mg L−1. The maximum specific ibuprofen removal rate and the value of the half-saturation constant were qmax = 0.24 ± 0.02 mg mL−1 h−1 and Ks = 2.12 ± 0.56 mg L−1, respectively. It has been suggested that monooxygenase and catechol 1,2-dioxygenase are involved in ibuprofen degradation by B. thuringiensis B1(2015b). Toxicity studies showed that B. thuringiensis B1(2015b) is more resistant to ibuprofen than other tested organisms. The EC50 of ibuprofen on the B1 strain is 809.3 mg L−1, and it is 1.5 times higher than the value of the microbial toxic concentration (MTCavg). The obtained results indicate that B. thuringiensis B1(2015b) could be a useful tool in biodegradation/bioremediation processes.

No MeSH data available.


Kinetic models of ibuprofen degradation (a) and bacterial survival (b) in the monosubstrate system and ibuprofen degradation (c) and bacterial growth (d) in the cometabolic system with glucose as a growth substrate. The data points represent the average of three independent experiments
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Fig2: Kinetic models of ibuprofen degradation (a) and bacterial survival (b) in the monosubstrate system and ibuprofen degradation (c) and bacterial growth (d) in the cometabolic system with glucose as a growth substrate. The data points represent the average of three independent experiments

Mentions: Despite the large amount of information about degradation of ibuprofen by the pure bacterial culture or microbial consortia, the kinetic model of ibuprofen degradation by the pure bacterial strain has not been described. For that reason, kinetic analysis of ibuprofen degradation by B. thuringiensis B1(2015b) was performed in monosubstrate or cometabolic systems with glucose as a growth substrate. The dependence of the specific ibuprofen removal rate on the ibuprofen concentration in monosubstrate and cometabolic systems is shown in panels a and c of Fig. 2, respectively. The half-saturation constant (Ks) and the maximum specific ibuprofen removal rate (qmax) were higher for the cometabolic system (Ks = 2.12 ± 0.56 mg L−1; qmax = 0.24 ± 0.02 mg L−1 h−1) than for the monosubstrate system (Ks = 0.68 ± 0.08 mg L−1; qmax = 0.09 ± 0.00 mg L−1 h−1). The half-saturation constant expresses a bacterial affinity for a substrate (Kim et al. 2003). Therefore, the lower Ks obtained for the monosubstrate system suggests that B. thuringiensis B1(2015b) is able to degrade ibuprofen faster at lower concentrations. The obtained results also showed that the introduction of an additional carbon source has a positive effect on ibuprofen degradation by B. thuringiensis B1(2015b). The increased degradation of a xenobiotic compound in the presence of an additional growth substrate was observed by Durruty et al. (2011). In their work, the simultaneous degradation of various chlorophenols was a key factor improving the degradation of pentachlorophenol (Durruty et al. 2011). The inhibitory effect of the substrate on its degradation is frequently observed. For example, Sinha et al. (2011) described the inhibition of degradation by the substrate during cultivation of Rhodococcus sp. RSP8 in the presence of phenol or p-chlorophenol. During our studies on degradation of ibuprofen by strain B1(2015b) in both monosubstrate and cometabolic cultures, the inhibition of this process by the substrate was also observed. In the monosubstrate system, inhibition was observed at a lower concentration of ibuprofen (6 mg L−1) than in the cometabolic system (9 mg L−1) (Fig. 2a, c). This was likely caused by bacterial cell death observed in the monosubstrate system (Fig. 2b). The initial death rate of 0.0003 ± 0.0002 increased to 0.44 ± 0.07. The kinetics of microbial death indicates that ibuprofen is an insufficient carbon source for bacteria. In turn, in the cometabolic system, the growth of bacterial cells was observed (Fig. 2d). In the presence of glucose as an additional carbon source, the maximum specific growth rate was 0.07 ± 0.01 mg mL−1 h−1, Ksμ was 0.27 ± 0.15 mg L−1 and Ki was 137.16 mg L−1. The increase of the maximum specific ibuprofen removal rate in the cometabolic system results from the high microbial biomass. In turn, the high half-saturation constant observed under cometabolic conditions may be connected with the competition between enzymes involved in ibuprofen degradation and those engaged in glucose metabolism for the cofactors.Fig. 2


Toxicity and biodegradation of ibuprofen by Bacillus thuringiensis B1(2015b)
Kinetic models of ibuprofen degradation (a) and bacterial survival (b) in the monosubstrate system and ibuprofen degradation (c) and bacterial growth (d) in the cometabolic system with glucose as a growth substrate. The data points represent the average of three independent experiments
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Related In: Results  -  Collection

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Fig2: Kinetic models of ibuprofen degradation (a) and bacterial survival (b) in the monosubstrate system and ibuprofen degradation (c) and bacterial growth (d) in the cometabolic system with glucose as a growth substrate. The data points represent the average of three independent experiments
Mentions: Despite the large amount of information about degradation of ibuprofen by the pure bacterial culture or microbial consortia, the kinetic model of ibuprofen degradation by the pure bacterial strain has not been described. For that reason, kinetic analysis of ibuprofen degradation by B. thuringiensis B1(2015b) was performed in monosubstrate or cometabolic systems with glucose as a growth substrate. The dependence of the specific ibuprofen removal rate on the ibuprofen concentration in monosubstrate and cometabolic systems is shown in panels a and c of Fig. 2, respectively. The half-saturation constant (Ks) and the maximum specific ibuprofen removal rate (qmax) were higher for the cometabolic system (Ks = 2.12 ± 0.56 mg L−1; qmax = 0.24 ± 0.02 mg L−1 h−1) than for the monosubstrate system (Ks = 0.68 ± 0.08 mg L−1; qmax = 0.09 ± 0.00 mg L−1 h−1). The half-saturation constant expresses a bacterial affinity for a substrate (Kim et al. 2003). Therefore, the lower Ks obtained for the monosubstrate system suggests that B. thuringiensis B1(2015b) is able to degrade ibuprofen faster at lower concentrations. The obtained results also showed that the introduction of an additional carbon source has a positive effect on ibuprofen degradation by B. thuringiensis B1(2015b). The increased degradation of a xenobiotic compound in the presence of an additional growth substrate was observed by Durruty et al. (2011). In their work, the simultaneous degradation of various chlorophenols was a key factor improving the degradation of pentachlorophenol (Durruty et al. 2011). The inhibitory effect of the substrate on its degradation is frequently observed. For example, Sinha et al. (2011) described the inhibition of degradation by the substrate during cultivation of Rhodococcus sp. RSP8 in the presence of phenol or p-chlorophenol. During our studies on degradation of ibuprofen by strain B1(2015b) in both monosubstrate and cometabolic cultures, the inhibition of this process by the substrate was also observed. In the monosubstrate system, inhibition was observed at a lower concentration of ibuprofen (6 mg L−1) than in the cometabolic system (9 mg L−1) (Fig. 2a, c). This was likely caused by bacterial cell death observed in the monosubstrate system (Fig. 2b). The initial death rate of 0.0003 ± 0.0002 increased to 0.44 ± 0.07. The kinetics of microbial death indicates that ibuprofen is an insufficient carbon source for bacteria. In turn, in the cometabolic system, the growth of bacterial cells was observed (Fig. 2d). In the presence of glucose as an additional carbon source, the maximum specific growth rate was 0.07 ± 0.01 mg mL−1 h−1, Ksμ was 0.27 ± 0.15 mg L−1 and Ki was 137.16 mg L−1. The increase of the maximum specific ibuprofen removal rate in the cometabolic system results from the high microbial biomass. In turn, the high half-saturation constant observed under cometabolic conditions may be connected with the competition between enzymes involved in ibuprofen degradation and those engaged in glucose metabolism for the cofactors.Fig. 2

View Article: PubMed Central - PubMed

ABSTRACT

In recent years, the increased intake of ibuprofen has resulted in the presence of the drug in the environment. This work presents results of a study on degradation of ibuprofen at 25 mg L−1 in the presence of glucose, as an additional carbon source by Bacillus thuringiensis B1(2015b). In the cometabolic system, the maximum specific growth rate of the bacterial strain was 0.07 ± 0.01 mg mL−1 h−1 and Ksμ 0.27 ± 0.15 mg L−1. The maximum specific ibuprofen removal rate and the value of the half-saturation constant were qmax = 0.24 ± 0.02 mg mL−1 h−1 and Ks = 2.12 ± 0.56 mg L−1, respectively. It has been suggested that monooxygenase and catechol 1,2-dioxygenase are involved in ibuprofen degradation by B. thuringiensis B1(2015b). Toxicity studies showed that B. thuringiensis B1(2015b) is more resistant to ibuprofen than other tested organisms. The EC50 of ibuprofen on the B1 strain is 809.3 mg L−1, and it is 1.5 times higher than the value of the microbial toxic concentration (MTCavg). The obtained results indicate that B. thuringiensis B1(2015b) could be a useful tool in biodegradation/bioremediation processes.

No MeSH data available.