Endocrine-disrupting chemicals are highly resistant organic compounds, commonly occurring in the aquatic environment, that can interfere with the endocrine system of animals and humans, causing serious chronic diseases. In recent decades, enzymes from oxidoreductases have been studied for their potential to degrade these compounds effectively. In order to use such enzymes repeatedly, it is necessary to ensure their insolubility in water, a method termed enzyme immobilization. We developed novel polyamide/polyethylenimine (PA/PEI) nanofibers as a promising support material for the immobilization of various biomolecules. Our nanofibers are highly suitable due to a unique combination of mechanical endurance provided by polyamide 6 and their affinity toward biomolecules, ensured by numerous PEI amino groups. Enzyme laccase was successfully immobilized onto PA/PEI nanofibers using a simple and fast method, providing exceptional activity and stability of the attached enzyme. We then tested the degradation ability of the PA/PEI-laccase samples on a highly concentrated mixture of endocrine-disrupting chemicals in real wastewater with adjusted pH. The results indicate that the samples were a suitable material for wastewater treatment by degrading a highly concentrated mixture of bisphenol A, 17α-ethinylestradiol, triclosan, and diclofenac, in real wastewater effluent.

We hypothesized that muscarinic receptors (MRs) in the heart have a role in stress responses and thus investigated changes in MR signaling (gene expression, number of receptors, adenylyl cyclase (AC), phospholipase C (PLC), protein kinase A and C (PKA and PKC) and nitric oxide synthase [NOS]) in the left ventricle, together with telemetric measurement of heart rate (HR) in mice (wild type [WT] and M2 knockout [KO]) during and after one (1R) or seven sessions (7R) of restraint stress (seven mice per group). Stress decreased M2 MR mRNA and cell surface MR in the left ventricle in WT mice. In KO mice, 1R, but not 7R, decreased surface MR. Similarly, AC activity was decreased in WT mice after 1R and 7R, whereas in KO mice, there was no change. PLC activity was also decreased after 1R in WT and KO mice. This is in accord with the concept that cAMP is a key player in HR regulation. No change was found with stress in NOS activity. Amount of AC and PKA protein was not changed, but was altered for PKC isoenzymes (PKCα, β, γ, η and ϵ (increased) in KO mice, and PKCι (increased) in WT mice). KO mice were more susceptible to stress as shown by inability to compensate HR during 120 min following repeated stress. The results imply that not only M2 but also M3 are involved in stress signaling and in allostasis. We conclude that for a normal stress response, the expression of M2 MR to mediate vagal responses is essential.

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