Significance and Impact of the Study: This study focused on the effect of rare earth (REs) on the biodegradation of polycyclic aromatic hydrocarbons (PAHs). The RE ions Ce³⁺ and Y³⁺ inhibited Moraxella osloensis CFP312 from degrading phenanthrene without affecting its glucose utilization. This inhibition effect can be relieved through co-cultivation with Bacillus subtilis MSP117, which has high adsorption capacity for RE ions in liquid and slurry systems. MSP117 adsorbed and fixed RE ions on its cell surfaces, thereby reducing the bioavailability of RE ions. This study provides a feasible way for the bioremediation of the co-pollution of RE and organic pollutants.

Abstract

The biodegradation of polycyclic aromatic hydrocarbons (PAHs) by micro-organisms in the environment is often inhibited by coexisting metal ions. The aim of this work is to study a bacterial consortium for enhancing phenanthrene biodegradation under the inhibition effect of the rare earth (RE) ions Ce³⁺ and Y³⁺. This bacterial consortium was composed of two bacteria, namely, the RE-adsorbing Bacillus subtilis MSP117 and the phenanthrene-degrading Moraxella osloensis CFP312. Ce³⁺ and Y³⁺ at the concentration of 1·15 mmol l⁻¹ inhibited CFP312 from degrading phenanthrene but not glucose. Using glucose as a co-substrate could promote the proliferation of CFP312 but decreased phenanthrene degradation. Adsorption experiments and electron microscopy imaging showed that CFP312 had no RE ions adsorption capacity for RE ions and that RE elements could not be observed on its cell surfaces. MSP117 could adsorb 0·14 and 0·12 mmol g⁻¹ wet cells of Ce³⁺ and Y³⁺ in aqueous solution, respectively, thus demonstrating considerable adsorption capacity. The MSP117 cell surface immobilized part of the free RE ions and reduced their bioaccessibility, thereby alleviating their biotoxic effect on phenanthrene degradation by CFP312. In liquid and slurry systems, glucose, which was used as the co-substrate of the bacterial consortium, must be kept at a low level to avoid the catabolism repression of phenanthrene degradation by CFP312.