Nitrile hydratase from Pseudomonas putida NRRL-18668 has been purified and characterized. The purified enzyme catalyzes the hydration of 2(S)-(4'-chlorophenyl)-3-methylbutyronitrile at least fifty times faster than that of 2(R)-(4'-chlorophenyl)-3-methylbutyronitrile. This enzyme is a member of the class of nitrile hydratase that contains cobalt. Visible absorption and CD spectra suggest the cobalt exists as a non-corrin low-spin Co3+ ion in a tetragonally-distorted octahedral ligand field. Chemical reduction of the native enzyme results in a species with the EPR signature of a low-spin Co2+ complex. Like the other cobalt-containing nitrile hydratases, this enzyme is relatively stable, maintaining its activity below 35 degrees C, and it shows a broad activity optimum between pH 7.2 and 7.8. The structural genes for this enzyme have been cloned and sequenced. The deduced amino acid sequences for the alpha and beta subunits show 48-63% and 35-41% homology, respectively, to other sequenced nitrile hydratases. In particular, the cysteine residues in the alpha subunit that have been suggested to coordinate the metal ion in the iron-containing nitrile hydratases [Brennan, B. A., Cummings, J. G., Chase, D. B., Turner, I. M., Jr., & Nelson, M. J. (1996) Biochemistry 35, 10068-10077] are conserved in this enzyme, suggesting that this nitrile hydratase, like the enzyme from Rhodococcus rhodochrous J1, is a member of a newly described class of metalloenzymes with Co3+-thiolate ligation [Brennan, B. A., Alms, G., Nelson, M. J., Durney, L. T., & Scarrow, R. C. (1996) J. Am. Chem. Soc. 118, 9194-9195].

Paracetamol (4′-hydroxyacetanilide, N-acetyl-paminophenol, acetaminophen, and paracetamol) is a widely used over-the-counter analgesic and antipyretic drug. Paracetamol and structural analogs are ubiquitous in the natural environment and easily accumulate in aquatic environment, which have been detected in surface waters, wastewater, and drinking water throughout the world. Paracetamol wastewater is mainly treated by chemical oxidation processes. Although these chemical methods may be available for treating these pollutants, the harsh reaction conditions, the generation of secondary pollutants, and the high operational cost associated with these methods have often made them not a desirable choice. Biodegradation of paracetamol is being considered as an environmentally friendly and low-cost option. The goal of this review is to provide an outline of the current knowledge of biodegradation of paracetamol in the occurrence, degrading bacteria, and proposed metabolic/ biodegrading pathways, enzymes and possible intermediates. The comprehensive understanding of the metabolic pathways and enzyme systems involved in the utilization of paracetamol means will be helpful for optimizing and allowing rational design of biodegradation systems for paracetamol-contaminated wastewater.

Microplastics (MPs) pollution is a global paradigm that raises concern in relation to environment and human health. In order to investigate the molecular toxicity mechanisms of MPs, transcriptomic analyses were performed on in vitro Caco‐2 cell model. After observing that polystyrene microplastics (PS‐MPs) decreased cell viability in a dose‐dependent manner, the responsible genes and involved pathways that might make contribution to PS‐MBs‐induced toxicity to Caco‐2 cells were identified with Illumina RNA seq. A total of 442 genes including, 210 up‐regulated ones and 232 down‐regulated ones, showed differential expression after treatment by PS‐MPs with a concentration of 12.5 mg L−1 or 50.0 mg L−1 for 24 hours. Gene Ontology (GO) annotation enriched unigenes can be grouped into three separated clusters: cellular component (CC), biological process (BP), and molecular function (MF). The dominate pathways related to NF‐κB, MAPK signaling, cytokine‐cytokine receptor interaction, and toll‐like receptor were strongly influenced by PS‐MBs. These pathways are involved in modulating cell inflammatory and proliferation. The qPCR were applied to investigate the transcriptional level of five proliferation related genes (Ras, ERK, MER, CDK4, Cyclin D1) and four inflammation related genes (TRPV1, iNOS, IL‐1β, IL‐8), and the results were consistent with RNA‐seq data. This study has provided new insight into the understanding of the toxicity effects of PS‐MBs‐induced intestinal inflammatory diseases.

This review aims to rationalize the existing functions of Nrf2 in chemoprevention and tumorigenesis, as well as the somatic mutations of Nrf2 and Keap1 in cancer and Nrf2 cross talk with miRNAs. This review also discusses the future challenges in Nrf2 research.