Competing charge transfer pathways at the photosystem II-electrode interface.

The integration of the water-oxidation enzyme photosystem II (PSII) into electrodes allows the electrons extracted from water oxidation to be harnessed for enzyme characterization and to drive novel endergonic reactions. However, PSII continues to underperform in integrated photoelectrochemical systems despite extensive optimization efforts. Here we carried out protein-film photoelectrochemistry using spinach and Thermosynechococcus elongatus PSII, and we identified a competing charge transfer pathway at the enzyme-electrode interface that short-circuits the known water-oxidation pathway. This undesirable pathway occurs as a result of photo-induced O2 reduction occurring at the chlorophyll pigments and is promoted by the embedment of PSII in an electron-conducting fullerene matrix, a common strategy for enzyme immobilization. Anaerobicity helps to recover the PSII photoresponse and unmasks the onset potentials relating to the QA/QB charge transfer process. These findings impart a fuller understanding of the charge transfer pathways within PSII and at photosystem-electrode interfaces, which will lead to more rational design of pigment-containing photoelectrodes in general.This work was supported by the U.K. Engineering and Physical Sciences Research Council (EP/H00338X/2 to E. Reisner), the U.K. Biology and Biotechnological Sciences Research Council (BB/K010220/1 to E. Reisner), a Marie Curie International Incoming Fellowship (PIIF-GA-2012-328085 RPSII to J.J.Z.). N.P. was supported by the Winton Fund for the Physics of Sustainability. E. Romero. and R.v.G. were supported by the VU University Amsterdam, the Laserlab-Europe Consortium, the TOP grant (700.58.305) from the Foundation of Chemical Sciences part of NWO, the Advanced Investigator grant (267333, PHOTPROT) from the European Research Council, and the EU FP7 project PAPETS (GA 323901). R.v.G. gratefully acknowledges his `Academy Professor' grant from the Royal Netherlands Academy of Arts and Sciences (KNAW). We would also like to thank Miss Katharina Brinkert and Prof A. William Rutherford for a sample of T. elongatus PSII, and H. v. Roon for preparation of the spinach PSII samples

Exposure to bisphenol A enhanced lung eosinophilia in adult male mice

Background: Bisphenol A (BPA) is useful in many manufacturing processes and is also found in commonly used consumer products. Previous experimental studies have reported that perinatal exposure to BPA promotes the development of allergic lung inflammation in childhood and even into adulthood. In this study, the effects of BPA on allergic lung inflammation in adults were investigated in murine lungs. Methods: CD-1 mice were orally administrated with 1 mg of BPA/mouse four times at one-week intervals with or without ovalbumin (OVA). The pathologic changes in the airways, cytological alterations in bronchoalveolar lavage fluid (BALF), levels of inflammatory cytokines/chemokines in BALF, and OVA-specific IgE and IgG1 antibodies in serum were measured in the treated CD-1 mice. In vitro study using RAW264.7 cells, which are macrophage-like cells derived from BALB/c male mice, was conducted. The gene expression of cytokines and chemokines were measured. Results: BPA enhanced eosinophil recruitment induced by OVA in the alveoli and in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. BPA increased Th2 cytokines-interleukin-13 (IL-13), eosinophil-relevant cytokines and chemokines, such as IL-5, and CCL2 induced by OVA, in BALF. BPA induced adjuvant effects on OVA-specific IgG1 production. In the in vitro study using RAW264.7 cells, BPA increased the mRNA expression of IL-1β, IL-6, CCL2 and CCL3 compared with the control and OVA groups. Conclusions: These results suggest that (1) the exposure of BPA could synergize with an OVA challenge to aggravate the severity of lung eosinophilia in adult mice, possibly by promoting a Th2-biased immune response and (2) the activation of macrophages and inflammatory cytokines released from these cells by BPA could be participating in this phenomenon