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We have performed first‐principle density functional theory calculations to investigate O2 dissociation on Pt(111) surface. A stepwise mechanism has been proposed. First, the adsorbed O2 dissociate into two oxygen atoms to get adsorbed on the nearby adsorption sites. Then, oxygen atoms further migrate to other more stable adsorption sites. The influence of solvent water on oxygen dissociation was also examined. The results show that the co‐adsorption of water has little impact on O2 dissociation. However, when water participates in the reaction, the energy barriers were reduced greatly. These results have very important significance to understand the mechanism of oxygen reduction. © 2016 Wiley Periodicals, Inc.

Procymidone (PCM) is a low toxicity fungicide, and an endocrine‐disrupting chemical (EDC) that particularly damages the reproductive system of male vertebrates. In present study, adolescent mice in control, low‐, medium‐, and high‐dose groups were orally administered 0 (equal volume of soybean oil), 50, 100, and 200 mg/kg/day PCM, respectively, for 21 days. Additionally, a three‐dimensional culture of mouse testes was performed in vitro, and the control, low dose (0.33 × 10−5 M), medium dose (1 × 10−5 M), and high dose (3 × 10−5 M) PCM groups were established. We have found that, under both in vivo and in vitro conditions, all doses of PCM caused damage to mouse testes. Moreover, the levels of circZc3h4 RNA and Zc3h4 decreased while miR‐212 increased in all treatment groups, with a corresponding rise in circRNA Scar and fall in Atp5b, compared to those in the control group, and all the changes showed a dose–response relationship. Besides, we have identified that low doses of PCM could activate the Ire1‐Xbp1 pathway, whereas the medium and high doses activated the Perk‐Elf2α‐Atf4, Ire1‐Xbp1, and Atf6 pathways. And it is, therefore, speculated that the unfolded protein response (UPR), circZc3h4 and circRNA Scar may have taken joint action in testicular injury in adolescent mice induced by PCM at the no observed adverse effect level (NOAEL, 100 mg/kg/day) and below NOAEL doses.

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Endothelin-1 (ET-1) is a powerful endogenous vasoconstrictor and it is closely related to the pathogenesis of endothelial dysfunction that is commonly involved in the initiation of vascular inflammation and in the development of vascular diseases. A new method for the electrochemical immunoassay of ET-1 was put forward in this work. ET-1 antibodies (Ab), gold nanoparticles (GNPs), and copper ions were employed to synthesize nanoenzyme-labeled antibodies, Ab-GNPs-Cu(II) nanocomposites, and the latter was evaluated using transmission electron microscopy, dynamic light scattering, UV−vis absorption spectrophotometry, Fourier transform infrared spectroscopy, and X-ray photoelectron spectroscopy. These nanocomposites could be captured on a glassy carbon electrode (GCE) modified with poly(thionine) (PTH) and ET-1, GCE/PTH/ET-1. The immobilized nanoenzymes, GNPs-Cu(II) nanoparticles, played a peroxidase mimic role. Hydroxyl radicals, • OH, generated by a Fenton-type reaction, oxidized PTH and induced the considerable cathodic current on an assembled sandwich-type electrode. Owing to the competitive immunoreaction, ET-1 in the solution inhibited the capture of Ab-GNPs-Cu(II) nanocomposites. The deficiency of • OH caused the decline of the electrochemical response. The cathodic current change was in proportion to the ET-1 concentration from 0.5 to 500 ng mL −1 . Cell morphology and viability investigations show that human umbilical vein endothelial cells, HUVECs, suffered from dysfunction when they were incubated in the presence of high-concentration glucose. Analyses on the growth medium using the developed method reveal that ET-1 was secreted by the injured cells and the release level of ET-1 was associated positively with the glucose concentration in the growth medium.

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