Selecting resonances in molecular scattering by anti-Zeno effect.

Utilizing the anti-Zeno effect, we demonstrate that the resonances of ultracold molecular interactions can be selectively controlled by modulating the energy levels of molecules with a dynamic magnetic field. We show numerically that the inelastic scattering cross section of the selected isotopic molecules in the mixed isotopic molecular gas can be boosted for 2-3 orders of magnitude by modulation of Zeeman splittings. The mechanism of the resonant anti-Zeno effect in the ultracold scattering is based on matching the spectral modulation function of the magnetic field with the Floquet-engineered resonance of the molecular collision. The resulting insight provides a recipe to implement resonant anti-Zeno effect in control of molecular interactions, such as the selection of reaction channels between molecules involving shape and Feshbach resonances, and external field-assisted separation of isotopes.

Channel Selection of Ultracold Atom-Molecule Scattering in Dynamic Magnetic Fields.

We demonstrate that final states of ultracold molecules by scattering with atoms can be selectively produced using dynamic magnetic fields of multiple frequencies. We develop a multifrequency Floquet coupled channel method to study the channel selection by dynamic magnetic field control, which can be interpreted by a generalized quantum Zeno effect for the selected scattering channels. In particular, we use an atom-molecule spin-flip scattering to show that the transition to certain final states of the molecules in the inelastic scattering can be suppressed by engineered coupling between the Floquet states.

Anthropogenic activities and coastal environmental quality: a regional quantitative analysis in southeast China with management implications.

Regional analysis of environmental issues has always been a hot topic in the field of sustainable development. Because the different levels of economic growth, urbanization, resource endowments, etc. in different regions generate apparently different ecological responses, a better description and comparison across different regions will provide more valuable implications for ecological improvement and policymaking. In this study, seven typical bays in southeast China that are a rapid developing area were selected to quantitatively analyze the relationship between socioeconomic development and coastal environmental quality. Based on the water quality data from 2007 to 2015, the multivariate statistical method was applied to analyze the potential environmental risks and to classify the seven bays based on their environmental quality status. The possible variation trends of environmental indices were predicted based on the cross-regional panel data by Environmental Kuznets Curve. The results showed that there were significant regional differences among the seven bays, especially Quanzhou, Xiamen, and Luoyuan Bays, suffered from severer artificial disturbances than other bays, despite their different development patterns. Socioeconomic development level was significantly associated with some water quality indices (pH, DIN, PO4-P); the association was roughly positive: the areas with higher GDP per capita have some worse water quality indices. In addition, the decreasing trend of pH values and the increasing trend of nutrient concentration in the seven bays will continue in the foreseeable future. In consideration of the variation trends, the limiting nutrient strategy should be implemented to mitigate the deterioration of the coastal environments.

Chromium alters lipopolysaccharide-induced inflammatory responses both in vivo and in vitro.

We demonstrated that pretreatment with chromium (Cr) significantly alters inflammatory responses of mice or macrophage cell lines. The mice were pretreated with 50 and 200 mg L(-1) of Cr dissolved in drinking water for 7 or 21 d, respectively. Then, the mice were challenged with lipopolysaccharide (LPS) or saline for 3 h. The body and liver weights significantly decreased after exposure to 200 mg L(-1) of Cr for both 7 and 21 d. Serious infiltration of inflammatory cells around the artery was found in the liver treated with 200 mg L(-1) of Cr for 7 and 21 d. The levels of tumor necrosis factor-α (TNFα) and interleukin-6 (IL6) in peritoneal macrophage significantly increased after the treatment with 200 mg L(-1) of Cr for 7 d. Moreover, LPS-induced increases in the serum levels and the transcriptional status of some cytokine genes were amplified by the Cr pretreatment. In the in vitro test, the RAW264.7 cell line was pretreated with Cr for 3, 6, 12, and 24 h, followed by stimulation with LPS (1 µg mL(-1)) for 6 h. LPS-induced the increases in TNFα, IL6, Interleukin-1α (IL1α), Interleukin-1ß (IL1ß), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX2) mRNA levels were significantly promoted by the pretreatment with Cr for 3, 6, and 12 h, whereas they were weakened by the pre-exposure to Cr for 24 h in a concentration-dependent manner. In addition, LPS-induced the release of TNFα and IL6 in the medium was also significantly enhanced or suppressed by the different Cr pretreatment. The results suggested that Cr had the potential to induce immunotoxicity by altering the inflammatory responses.

Cadmium exposure to murine macrophages decreases their inflammatory responses and increases their oxidative stress.

Cadmium (Cd) is an environmental contaminant that poses serious risks to human and wildlife health. The oxidative stress and inflammatory responses induced by Cd were evaluated in RAW264.7 cells. A significant decrease in the cell viability was observed in the group treated with 3 µM Cd for 24 h. The mRNA levels of tumor necrosis factor-α (TNFα), interleukin-6 (IL6), interleukin-1α (IL1α) and Interleukin-1ß (IL1ß) were generally increased or decreased by Cd exposure for 6 and 24 h, respectively. Moreover, pretreatment of the RAW264.7 cells with Cd for 24 h inhibited the transcriptional status of TNFα, IL6, IL1α and IL1ß and the release of these cytokines in response to a 6-h lipopolysaccharide (LPS) treatment in a dose-dependent manner. Furthermore, the Cd exposure elicited oxidative stress not only by disturbing the transcriptional status of genes including superoxide dismutase (Sod), catalase (Cat), glutathione peroxidase(Gpx), glutathione S-transferase 1 a (Gst1a), NAD(P)H: quinone oxidoreductase 1(Nqo1), heme oxygenase 1(Ho-1) but also the enzyme activities of SOD, CAT and glutathione S-transferase (GST). The effects of Cd on the mRNA levels and activities of anti-oxidative enzymes were dependent on the exposure period and dose. These results suggested that Cd exposure generated oxidative stress and decreased the inflammatory responses in a murine macrophage cell line. Furthermore, oxidative stress may be a possible mechanism to explain the dysregulation of the immune function caused by heavy metals in this in vitro system.

Oral exposure of mice to cadmium (II), chromium (VI) and their mixture induce oxidative- and endoplasmic reticulum-stress mediated apoptosis in the livers.

Health concerns regarding the environmental heavy metals in wildlife and humans have increased in recent years. We evaluated the effects of exposure of mice to low doses of cadmium (Cd), chromium (Cr) and their mixtures on oxidative- and ER-stress. Male adult mice were orally exposed to Cd (0.5 and 2 mg kg(-1) ), Cr (1 and 4 mg kg(-1) ) and binary Cd+Cr mixtures (0.25 + 05 and 1 + 2 mg kg(-1) ) daily for 36 days. We observed that the bioaccumulation of Cd and Cr in the liver in a dose-dependent manner, and the Cd and Cr contents in the 2 mg kg(-1) Cd and 4 mg kg(-1) Cr treated groups reached 2.43 and 3.46 µg g(-1) liver weight. In addition, treatments with 2 mg kg(-1) Cd, 4 mg kg(-1) Cr or their mixture (1 + 2 mg kg(-1) ) significantly decreased body and liver weights, increased the levels of reactive oxygen species (ROS), malondialdehyde (MDA) and activities of catalase (CAT) and glutathione peroxidase (GPX) in the liver. Moreover, Cd and Cr exposures also elevated the transcription of the oxidative- and endoplasmic reticulum (ER)-stress related genes including Cat, Gpx, heme oxygenase 1 (Ho-1), regulated protein 78 (Grp78), activating transcription factor 6 (Atf6) and proaoptotic CCAAT/-enhancer-binding protein homologous protein (Chop) in a dose dependent manner in the liver. And hepatic cytochrome c levels increased in all Cd, Cr or their mixture treated groups. Furthermore, the transcriptional status and the activities of Caspase 9 and Caspase 3 were increased significantly in the liver when exposed to high doses of Cd, Cr or their mixture. These results suggested that a long period exposure of mice to Cd or Cr has the potential to elicit oxidative- and ER-stress mediated apoptosis in their livers. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 693-705, 2016.

Subchronic Exposure of Mice to Cadmium Perturbs Their Hepatic Energy Metabolism and Gut Microbiome.

Cadmium (Cd) is an environmental pollutant known to cause liver damage; however, the mechanisms of its hepatotoxicity remain poorly understood. In this study, the effects of subchronic exposure in mice to low doses of Cd on energy metabolism and the gut microbiome were evaluated. The exposure of mice to 10 mg/L Cd supplied in drinking water for 10 weeks increased hepatic triacylglycerol (TG), serum free fatty acid (FFA), and TG levels. The mRNA levels of several key genes involved in both de novo FFA synthesis and transport pathways and in TG synthesis in the liver also increased significantly in the Cd-treated mice, indicating that alterations of these genes may be a possible mechanism to explain subchronic Cd exposure induced hepatic toxicity at a molecular level. As for the gut microbiome, at the phylum level, the amounts of Firmicutes and γ-proteobacteria decreased significantly in the feces after 4 weeks of Cd exposure, and the quantity of Firmicutes decreased significantly in the cecum contents after 10 weeks of Cd exposure. In addition, 16S rRNA gene sequencing further revealed that Cd exposure significantly perturbed the gut microflora structure and richness at family and genus levels. The alteration of gut microbiome composition might result in an increase in serum lipopolysaccharide (LPS) and induce hepatic inflammation, which may indirectly cause perturbations of energy homeostasis after Cd exposure. Taken together, the present study indicated that subchronic Cd exposure caused the dysregulation of energy metabolism and changed the gut microbiome composition in mice.

Oral Exposure of Mice to Carbendazim Induces Hepatic Lipid Metabolism Disorder and Gut Microbiota Dysbiosis.

Carbendazim (CBZ) has been considered as an endocrine disruptor that caused mammalian toxicity in different endpoints. Here, we revealed that oral administrations with CBZ at 100 and 500 mg/kg body weight for 28 days induced hepatic lipid metabolism disorder which was characterized by significant increases of hepatic lipid accumulation and triglyceride (TG) levels in mice. The serum cholesterol (TC), high-density lipoprotein, and low-density lipoprotein levels also increased after CBZ exposure. Correspondingly, the relative mRNA levels of some key genes related to lipogenesis and TG synthesis increased significantly both in the liver and fat. Moreover, the increase in serum IL-1ß and IL-6 levels by the treatment of CBZ indicated the occurring of inflammation. Furthermore, the levels of bioaccumulation of CBZ in the liver and gut were very low as compared in the feces, indicating that most of CBZ stayed in gastrointestinal tract and interacted with gut microbiota until excreted. At phylum level, the amounts of the Bacteroidetes decreased significantly in the feces after 5 days CBZ exposure. High throughput sequencing of the 16S rRNA gene V3-V4 region revealed a significant reduction in richness and diversity of gut microbiota in the cecum of CBZ-treated mice. UniFrac principal coordinates analysis observed a marked shift of the gut microbiota structure in CBZ-treated mice away from that of the controls. More deeply, operational taxonomic units' analysis identified that a total of 361 gut microbes were significant changed. In CBZ-treated groups, the relative abundance of Firmicutes, Proteobacteria, and Actinobacteria increased and that of Bacteroidetes decreased. Our findings suggested that CBZ could lead hepatic lipid metabolism disorder and gut microbiota dysbiosis in mice.

TPP and TCEP induce oxidative stress and alter steroidogenesis in TM3 Leydig cells.

Effects of triphenyl phosphate (TPP) and tris-(2-chloroethyl) phosphate (TCEP) exposure on induction of oxidative stress and endocrine disruption were investigated in TM3 cells. After 24h exposure, cell growth declined and morphology changed in TPP and TCEP treated groups with high dosages. Significant increases in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glutathione S-transferase (GST) activities and their respective gene expressions in a dose-dependent and/or time-dependent manner in TPP or TCEP groups. Moreover, the expression of main genes related to testosterone (T) synthesis including cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), cytochrome P450 17α-hydroxysteroid dehydrogenase (P450-17α), 3ß-hydroxysteroid dehydrogenase (3ß-HSD) and 17ß-hydroxysteroid dehydrogenase (17ß-HSD) were dramatically reduced by TPP and TCEP treatments, especially with the high dosage for 24h. TPP and TCEP treatments for 24h caused significant decreases in T levels in the medium. Furthermore, co-treatments of hCG with TPP or TCEP could inhibit hCG-induced changes in the expression of P450scc, P450-17α and 17ß-HSD and T levels. Taken together, TPP and TCEP could induce oxidative stress and endocrine disruption in TM3 cells.

Hepatic oxidative stress and inflammatory responses with cadmium exposure in male mice.

Cadmium (Cd), a non-essential heavy metal, is one of the major environmental contaminants with grave toxicological consequences globally. In the present study, the effects of Cd on hepatic oxidative stress and inflammatory responses in mice were evaluated. Male adult mice were orally exposed to 3, 10 and 30mg/L CdCl2 supplied in the drinking water for 7 and 21 days. Histopathological changes and the alterations of the main parameters related to oxidative stress and inflammatory responses in the liver were observed. Hepatic malondialdehyde (MDA) contents increased significantly after treatment with 30mg/L CdCl2 for 21 days, and the contents of glutathione (GSH) increased significantly in both 10 and 30mg/L CdCl2 treated groups. The hepatic activities of glutathione peroxidase (GPX), catalase (CAT) and glutathione S-transferase (GST) increased significantly after the treatment with 30mg/L CdCl2 for 21 days. In accordance with the enzyme activities, the transcription status of hepatic superoxide dismutase 1 (Sod1), superoxide dismutase 2 (Sod2), Cat, Gpx, Gstα1, glutathione synthetase (Gss), glutathione reductase (Gr) and heme oxygenase 1 (Ho1) were also increased by high dose (30mg/L) or long period (21 days) exposure. In addition, the serum levels of tumor necrosis factor α (TNFα), interleukin 6 (IL6) and interleukin 1ß (IL1ß) increased significantly in the groups treated with 30mg/L CdCl2 for 21 days. And the genes of TNFα, IL6, interleukin 1α (IL1α), inducible nitric oxide synthase (iNOS) and interferon γ (IFNγ) were also increased in the liver of mice when exposed to relative high dose of CdCl2 for 7 or 21 days. Taken together, the results of this study suggested that the exposure to Cd had the potential to induce immunotoxicity accompanied with oxidative stress in the liver of mice.