Oxidative decomposition mechanisms of lithium carbonate on carbon substrates in lithium battery chemistries.

Lithium carbonate plays a critical role in both lithium-carbon dioxide and lithium-air batteries as the main discharge product and a product of side reactions, respectively. Understanding the decomposition of lithium carbonate during electrochemical oxidation (during battery charging) is key for improving both chemistries, but the decomposition mechanisms and the role of the carbon substrate remain under debate. Here, we use an in-situ differential electrochemical mass spectrometry-gas chromatography coupling system to quantify the gas evolution during the electrochemical oxidation of lithium carbonate on carbon substrates. Our results show that lithium carbonate decomposes to carbon dioxide and singlet oxygen mainly via an electrochemical process instead of via a chemical process in an electrolyte of lithium bis(trifluoromethanesulfonyl)imide in tetraglyme. Singlet oxygen attacks the carbon substrate and electrolyte to form both carbon dioxide and carbon monoxide-approximately 20% of the net gas evolved originates from these side reactions. Additionally, we show that cobalt(II,III) oxide, a typical oxygen evolution catalyst, stabilizes the precursor of singlet oxygen, thus inhibiting the formation of singlet oxygen and consequent side reactions.

True Reaction Sites on Discharge in Li-O2 Batteries.

In the pursuit of an advanced Li-O2 battery, the true reaction sites in the cathode determined its cell performance and the catalyst design. When the first layer of insulating Li2O2 solid is deposited on the electrode substrate during discharging, the following O2 reduction to Li2O2 could take place either at the electrode|Li2O2 interface or at the Li2O2|electrolyte interface. The mechanism decides the strategies of catalyst design; however, it is still mysterious. Here, we used rotate ring-disk electrode to deposit a dense Li2O2 film and labeled the Li2O2 product with 16O/18O isotope. By identification of the distribution of the Li216O2 and Li218O2 in the Li2O2 film using new characteristic signals of Li216O2 and Li218O2, our results show that O2 is reduced to Li2O2 at both interfaces. A sandwich structure of Li218O2|Li216O2|Li218O2 was identified at the electrode surface when the electrode was discharged under 16O2 and then 18O2. The electrode|Li2O2 interface is the major reaction site, and it contributes to 75% of the overall reaction. This new mechanism raises new challenges and new strategies for the catalyst design of Li-O2 batteries.

Transgenerational male reproductive effect of prenatal arsenic exposure: abnormal spermatogenesis with Igf2/H19 epigenetic alteration in CD1 mouse.

Developmental exposure to environmental toxicants can induce transgenerational reproductive disease phenotypes through epigenetic mechanisms. We treated pregnant CD-1 (F0) mice with drinking water containing sodium arsenite (85 ppm) from days 8 to 18 of gestation. Male offspring were bred with untreated female mice until the F3 generation was produced. Our results revealed that F0 transient exposure to arsenic can cause decreased sperm quality and histological abnormalities in the F1 and F3. The overall methylation status of Igf2 DMR2 and H19 DMR was significantly lower in the arsenic-exposed group than that of the control group in both F1 and F3. The relative mRNA expression levels of Igf2 and H19 in arsenic-exposed males were significantly increased in both F1 and F3. This study indicates that ancestral exposure to arsenic may result in transgenerational inheritance of an impaired spermatogenesis phenotyping involving both epigenetic alterations and the abnormal expression of Igf2 and H19.

Redox Mediator-Enhanced Performance and Generation of Singlet Oxygen in Li-CO2 Batteries.

Rechargeable Li-CO2 batteries as a novel system developed in recent years directly use CO2 as the reactant, which enables deeper penetration of energy storage and CO2 utilization. The Li-CO2 battery system, however, is at an early stage, and many challenges remained to be overcome urgently, especially the problem of high over-potential during the charging process. Here, we report a redox mediator, phenoxathiin, to assist the decomposition of Li2CO3 during the charging process, which effectively reduces the over-potential and improves the cycling performance of the battery. Furthermore, we detect the presence of singlet oxygen during the oxidation of Li2CO3 by phenoxathiin, which reveals more of the underlying science of the reaction mechanism of the Li-CO2 battery.

Associations of urinary phenolic environmental estrogens exposure with blood glucose levels and gestational diabetes mellitus in Chinese pregnant women.

BACKGROUND: Endocrine-disrupting chemicals (EDCs) are considered to be related to diabetes, but studies of the association between phenolic EDCs and gestational diabetes mellitus (GDM) are limited. OBJECTIVES: To assess associations of maternal urinary bisphenol A (BPA), nonylphenol (NP), and 2-tert-octylphenol (2-t-OP) with GDM occurrence. METHODS: A cross-sectional study was performed among 390 Chinese women at 24-28 weeks of gestation. GDM was diagnosed with a 2-h 75-g oral glucose tolerance test (OGTT). BPA, NP, and 2-t-OP concentrations were determined in urine samples. Linear and logistic regression tests evaluated associations of BPA, NP, and 2-t-OP with blood glucose levels and GDM prevalence. RESULTS: The 2-t-OP concentrations in GDM patients were significantly higher than in non-GDM women with median values of 2.23 µg/g Cr and 1.79 µg/g Cr, respectively. No significant difference was observed in BPA and NP. Urinary 2-t-OP was positively associated with blood glucose levels after adjustment for several confounding factors and urinary BPA and NP. Higher 2-t-OP levels were associated with higher odds of GDM (OR: 5.78; 95% CI: 2.04, 16.37), whereas higher NP levels were associated with lower odds (OR: 0.22; 95% CI: 0.05, 0.85) in the adjusted models. In addition, compared to the first quartile of 2-t-OP, the adjusted odds ratios (ORs) and 95% confidence intervals (95% CIs) for GDM in the second, third, and fourth quartiles were 2.81 (1.23, 6.42), 3.01 (1.30, 6.93), and 5.49 (2.24, 13.46), respectively. CONCLUSION: Our study indicates that, for the first time to our knowledge, exposure to 2-t-OP is associated with a higher risk of GDM. However, higher NP exposure is associated with lower GDM risk. Further studies are necessary to affirm the associations of 2-t-OP and NP with GDM, and to elucidate the causality of these findings.

ß-cypermethrin-induced acute neurotoxicity in the cerebral cortex of mice.

A Type II pyrethroid pesticide ß-cypermethrin is widely used in agriculture and domestic applications for pest control. However, the effect of ß-cypermethrin on the glutamate neurotransmitter has not been well-documented. In the current study, mice were treated with 20, 40, or 80 mg/kg ß-cypermethrin by a single oral gavage, with corn oil as a vehicle control. Four hours after treatment, we investigated glutamate levels and glutamate-metabolizing enzyme (phosphate-activated glutaminase, PAG; glutamine synthetase, GS) activities in the cerebral cortex of mice, using a HPLC system with ultraviolet detectors and a colorimetric assay. Glutamate uptake levels in the synaptosomes of cerebral cortex and mRNA expression levels of PAG, GS, and glutamate transporter-1 (GLT-1) in the cerebral cortex were detected by a radioactive labeling method and qRT-PCR, respectively. Toxic symptoms were observed in mice treated with 40 or 80 mg/kg ß-cypermethrin. Compared with the control, significant decreases in glutamate level and GS activity, and an obvious increase in synaptosomal glutamate uptake, were found in the cerebral cortex of mice treated with 80 mg/kg ß-cypermethrin. No significant changes were found among groups in PAG activity or PAG, GS, and GLT-1 mRNA expression levels. These results suggest that ß-cypermethrin treatment may reduce the glutamate level in the mouse cerebral cortex, which is associated with decreased GS activity and increased synaptosomal glutamate uptake. Our findings provide a partial explanation for the neurotoxic effects of synthetic ß-cypermethrin insecticides.