Microbial-induced carbonate precipitation effectively prevents Pb2+ migration through the soil profile: Lab experiment and model simulation.

Due to the inappropriate disposal of waste materials containing lead (Pb) and irrigation with sewage containing Pb, the migration of Pb2+ within the soil profile has been extensively investigated. The conventional Pb2+ block method is challenging to implement due to its complex operational procedures and high construction costs. To address this issue, this study introduces the microbial-induced carbonate precipitation (MICP) technique as a novel approach to impede the migration of Pb2+ in the soil profile. Soil acclimatization with urea resulted in an increased proportion of urease-producing microorganisms, including Bacillus, Paenibacillus, and Planococcaceae, along with heightened expression of urea-hydrolyzing genes (UreA, UreB, UreC, and UreG). This indicates that urea-acclimatized soil (Soil-MICP) possesses the potential to induce carbonate precipitation. Batch Pb2+ fixation experiments confirmed that the fixation efficiency of Soil-MICP on Pb2+ exceeded that of soil without MICP, attributed to the MICP process within the Soil-MICP group. Dynamic migration experiments revealed that the MICP reaction transformed exchangeable lead into carbonate-bound Pb, effectively impeding Pb2+ migration in the soil profile. Additionally, the migration rate of Pb2+ in Soil-MICP was influenced by varying urea amounts, pH levels, and pore flow rates, leading to a slowdown in migration. The Two-site sorption model aptly described the Pb2+ migration process in the Soil-MICP column. This study aims to elucidate the MICP biomineralization process, uncover the in-situ blocking mechanism of MICP on lead in soil, investigate the impact of Pb on key genes involved in urease metabolism, enhance the comprehension of the chemical morphology of lead mineralization products, and provide a theoretical foundation for MICP technology in preventing the migration of Pb2+ in soil profiles.

Application of microbial-induced carbonate precipitation (MICP) techniques to remove heavy metal in the natural environment: A critical review.

The occurrence of imbalanced heavy metals concentration due to anthropogenic hindrances in the aquatic and terrestrial environment has become a potential risk to life after circulating through different food chains. The microbial-induced carbonate precipitation (MICP) method has gradually received great attention from global researchers but the underlying mechanism of heavy metal mineralization is not well-understood and challenging, limiting the applications in wastewater engineering. This paper reviews the metabolic pathways, mechanisms, operational factors, and mathematical/modeling approaches in the MICP process. Subsequently, the recent advancement in MICP for the remediation of heavy metal pollution is being discussed. In the follow-up, the key challenges and prospective associated with technical bottlenecks of MICP method are elaborated. The prospective study reveals that MICP technology could be efficiently used to remediate heavy metal contaminants from the natural environment in a cost-effective way and has the potential to improve soil properties while remediating heavy metal contaminated soil.

Delayed induction of delta-6 and delta-5 desaturases by a peroxisome proliferator.

Delta-6 desaturase (D6D) is the key enzyme for the synthesis of highly unsaturated fatty acids (HUFA) such as arachidonic acid (AA) and docosahexaenoic acid (DHA) in mammals. Transcription of D6D gene is activated by both sterol regulatory element binding protein-1c (SREBP-1c) and peroxisome proliferators (PP). This response of D6D is paradoxical because SREBP-1c transactivates genes for fatty acid synthesis in liver, while PP induce enzymes for fatty acid oxidation. We hypothesized that the induction of D6D gene by PP is a compensatory response to the increased HUFA demand caused by peroxisome proliferation and induction of fatty acid oxidation. We investigated the time-course effects of a PP, Wy14643, on the induction of HUFA metabolizing genes and HUFA profile in rat liver. The mRNA of fatty acid oxidation enzymes in the Wy14643 fed group became significantly higher than controls at 4 h and reached maximum within 28 h. In contrast, the mRNA of delta-6 and delta-5 desaturases in the Wy14643 group was not significantly higher than control at 4 h and took >28 h to reach the maximum. Despite the induction of HUFA synthetic pathway, the concentration of end products (AA and DHA) remained unchanged throughout the 4-day period in liver phospholipids and non-esterified fatty acids. Taken together, this study supports our hypothesis and suggests that peroxisome proliferation and induction of fatty acid oxidation enzymes are the major mechanisms of the induction of HUFA synthesis by PP.