A Luminescent Cd-MOF Used as a Chemosensor for High-Efficiency Sensing of Fe3+, Cr(IV), Trinitrophenol, and Colchicine.

A Cd-MOF was constructed based on 3,5-bis(4-carboxyphenyl) pyridine under solvothermal conditions. Its structure and phase purity were verified by single-crystal X-ray diffraction. Thereafter, some studies on the morphology, structure, and luminescent properties of the compound were carried out. The compound exhibited a highly sensitive response to Fe3+, Cr(IV), trinitrophenol (TNP), and colchicine based on the fluorescence-quenching mechanism. The possible mechanism of luminescence quenching was discussed in detail.

Occurrence and dissemination of antibiotic resistance genes in the Yellow River basin: focused on family farms.

As an emerging contaminant, antibiotic resistance genes (ARGs) have attracted growing attention, owing to their widespread dissemination and potential risk in the farming environment. However, ARG pollution from family livestock farms in the Yellow River basin, one of the main irrigation water sources in the North China Plain, remains unclear. Herein, we targeted 21 typical family farms to assess the occurrence patterns of ARGs in livestock waste and its influence on ARGs in receiving environment by real-time quantitative PCR (qPCR). Results showed that common ARGs were highly prevalent in family livestock waste, and tet-ARGs and sul-ARGs were the most abundant in these family farms. Most ARG levels in fresh feces of different animals varied, as the trend of chicken farms (broilers > laying hens) > swine farms (piglets > fattening pigs > boars and sows) > cattle farms (dairy cattle > beef cattle). The effect of natural composting on removing ARGs for chicken manure was better than that for cattle manure, while lagoon storage was not effective in removing ARGs from family livestock wastewater. More troublesomely, considerable amounts of ARGs were discharged with manure application, further leading to the ARG increase in farmland soil (up to 58-119 times), which would exert adverse impacts on human health and ecological safety.

Porous Metal-Organic Frameworks for Light Hydrocarbon Separation.

The separation of light hydrocarbon compounds is an important process in the chemical industry. Currently, its separation methods mainly include distillation, membrane separation, and physical adsorption. However, these traditional methods or materials have some drawbacks and disadvantages, such as expensive equipment costs and high energy consumption, poor selectivity, low separation ratios, and separation efficiencies. Therefore, it is important to develop novel separation materials for light hydrocarbon separation. As a new type of organic-inorganic hybrid crystalline material, metal-organic frameworks (MOFs) are promising materials for light hydrocarbon separation due to their designability of structure and easy modulation of function. This review provides an overview of recent advances in the design, synthesis, and application of MOFs for light hydrocarbon separation in recent years, with a focus on the separation of alkane, alkene, and alkyne. We discuss strategies for improving the adsorption selectivity and capacity of MOFs, including pore size limitation, physical adsorption, and chemisorption. In addition, we discuss the advantages/disadvantages, challenges, and prospects of MOFs in the separation of light hydrocarbon.

Effect of HHCB and Cd on phytotoxicity, accumulation, subcellular distribution and stereoselectivity of chiral HHCB in soil-plant systems.

The toxicity of HHCB in the growth and development of plants is well known, but its uptake, subcellular distribution, and stereoselectivity, especially in a co-contamination environment, is not fully understood. Therefore, a pot experiment was performed to research the physiochemical response, and the fate of HHCB in pakchoi when the Cd co-existed in soil. The Chl contents were significantly lower, and the oxidative stress was aggravated under the co-exposure of HHCB and Cd. The accumulations of HHCB in roots were inhibited, and those in leaves were elevated. The transfer factors of HHCB in HHCB-Cd treatment increased. The subcellular distributions were analyzed in the cell walls, cell organelles, and cell soluble constituents of roots and leaves. In roots, the distribution proportion of HHCB followed cell organelle > cell wall > cell soluble constituent. In leaves, the distribution proportion of HHCB was different from that in roots. And the co-existing Cd made the distribution proportion of HHCB change. In the absence of Cd, the (4R,7S)-HHCB and (4R,7R)-HHCB were preferentially enriched in roots and leaves, and the stereoselectivity of chiral HHCB was more significant in roots than leaves. The co-existing Cd reduced the stereoselectivity of HHCB in plants. Our findings suggested that the fate of HHCB was affected by the co-existing Cd, so the risk of HHCB in the complicated environment should be paid more attention.

Kinesin spindle protein inhibitor exacerbates cisplatin-induced hair cell damage.

There is emerging evidence indicating that Kinesin family, plays vital roles in influencing the growth of axons, interference with the progression of tumor. However, the function of Kinesin member in the auditory organs remains unknown. SB743921, a kinesin spindle protein (KSP) inhibitor, was applied in mouse organ of Corti and House Ear Institute-Organ of Corti 1 (HEI-OC1) cell line to examine the role of KSP in auditory system with and without cisplatin damage. Cell Counting Kit-8 (CCK-8) and Lactase dehydrogenase (LDH) release assay were conducted to evaluate cell activity and toxicity. Pretreatment with SB743921 increased the sensitivity of HEI-OC1 cells to cisplatin ototoxicity through promoting cell apoptosis and deteriorating superoxide generation mediated damage from cisplatin. SB743921 also enhanced cisplatin induced hair cell damage in explants of mouse cochleae in vitro. Furthermore, the combined N-acetylcysteine (NAC) treatment with cisplatin or with cisplatin and SB743921 both completely rescued the reduced number of hair cells impaired by cisplatin, confirming the strengthening function of superoxide accumulation by SB743921 after cisplatin treatment. Inhibition of kinesin spindle protein enhanced the susceptibility of hair cells to cisplatin induced damage in mouse cochlear explants and HEI-OC1 cells, indicating that kinesin spindle protein might be an unprecedented target to weaken the ototoxicity of platinum medicaments.

Current Progress in Natural Degradation and Enhanced Removal Techniques of Antibiotics in the Environment: A Review.

Antibiotics are used extensively throughout the world and their presence in the environment has caused serious pollution. This review summarizes natural methods and enhanced technologies that have been developed for antibiotic degradation. In the natural environment, antibiotics can be degraded by photolysis, hydrolysis, and biodegradation, but the rate and extent of degradation are limited. Recently, developed enhanced techniques utilize biological, chemical, or physicochemical principles for antibiotic removal. These techniques include traditional biological methods, adsorption methods, membrane treatment, advanced oxidation processes (AOPs), constructed wetlands (CWs), microalgae treatment, and microbial electrochemical systems (such as microbial fuel cells, MFCs). These techniques have both advantages and disadvantages and, to overcome disadvantages associated with individual techniques, hybrid techniques have been developed and have shown significant potential for antibiotic removal. Hybrids include combinations of the electrochemical method with AOPs, CWs with MFCs, microalgal treatment with activated sludge, and AOPs with MFCs. Considering the complexity of antibiotic pollution and the characteristics of currently used removal technologies, it is apparent that hybrid methods are better choices for dealing with antibiotic contaminants.

Kif15 Is Required in the Development of Auditory System Using Zebrafish as a Model.

Kif15, a kinesin family member, is powerful in the formation of bipolar spindles. There is emerging evidence indicating that Kif15 plays vital roles in influencing the growth of axons and interference with the progression of the tumor. However, the function of Kif15 in the auditory organs remains unknown. The Western blotting test was used to examine the effect of Kif15 downregulation by specific morpholino targeting Kif15 (Kif15-MO). The development of the inner ear and posterior lateral line (PLL) system in zebrafish was under continuous observation from spawns to 96 h postfertilization (hpf) to investigate the potential role of Kif15 in the auditory and vestibular system. We uncovered that Kif15 inhibition induced otic organ deformities in zebrafish, including malformed semicircular canals, abnormal number and location of otoliths, and reduced number of hair cells (HCs) both in utricle and saccule. Furthermore, a remarkable reduction in the number of PLL neuromasts was also explored in Kif15-MO morphants compared to the normal larvae. We also detected notably reduced activity in locomotion after Kif15 was knocked down. Additionally, we performed rescue experiments with co-injection of Kif15 mRNA and found that the Kif15 splicing MO-induced deformities in otic vesicle and PLL of zebrafish were successfully rescued, and the severely reduced locomotor activity caused by Kif15-MO was partially rescued compared to the control-MO (Con-MO) embryos. Our findings uncover that Kif15 is essential in the early development of auditory and vestibular organs using zebrafish as models.

Dnmt1 is required for the development of auditory organs via cell cycle arrest and Fgf signalling.

OBJECTIVES: To explore the role of DNA methyltransferase 1 (DNMT1) in the development of auditory system using zebrafish as experimental model. METHODS: Morpholino oligonucleotide was used to induce Dnmt1 deficiency. RNA sequencing, in situ hybridization (ISH), whole genomic bisulfide sequencing (WGBS) and immunostaining were used to investigate the morphologic alterations and mechanisms. RESULTS: We found that downregulation of Dnmt1 induced decreased number of neuromasts and repressed cell proliferation of primordium in the developing posterior lateral line system of zebrafish. The ISH data uncovered that Fgf signalling pathway was inhibited and the expression of chemokine members cxcr4b, cxcr7b and cxcl12a were interfered, while lef1 expression was increased after inhibiting Dnmt1. Additionally, Dnmt1 downregulation led to malformed otoliths and deformed semicircular canals, and hair cell differentiation in utricle and saccule was inhibited severely. The in situ staining of otic placode markers pax2/5 and fgf 3/8/10 was decreased when Dnmt1 downregulated. The WGBS analysis demonstrated that the global methylation status was markedly downregulated, and cell cycle genes were among those most differently expressed between Dnmt1 morphants and the controls. Further ISH analysis confirmed the findings by RNA-seq and WGBS assay that cdkn1a and tp53 were both upregulated after knockdown of Dnmt1. CONCLUSION: Our results revealed that Dnmt1 is essential for the development of zebrafish auditory organ through regulating cell cycle genes together with Wnt and Fgf signalling pathways.

The protective effect of rutin against the cisplatin-induced cochlear damage in vitro.

Rutin is a natural flavonoid, with typical effects including interaction with enzymes and scavenging of free radicals. However, the role of rutin in the auditory system is still unclear. In the present study, we used neonatal organ of Corti explants in vitro to investigate the effects of rutin in cisplatin-induced ototoxicity. The TUNEL assay and the cleaved caspase-3 immunohistochemistry were used to detect the apoptosis of hair cell (HCs) in cochlear explants, and the MitoSox-Red staining was used to detect the difference in mitochondrial superoxide among different groups. Western blot was used to investigate the expression of genes. Confocal microscopy showed that after pretreatment with rutin, the accumulation of reactive oxygen species in HCs caused by cisplatin exposure was significantly reduced. Furthermore, the expression levels of p-P38 and p-JNK were significantly decreased, while ratio of p-AKT/AKT was significantly upregulated. Our study showed that rutin reduced cisplatin-induced HCs death in neonatal cochlear explants in vitro. The potential mechanism involved the alleviation of mitochondrial damage, the scavenging of reactive oxygen species (ROS), the suppression of MAPK signaling pathway, and the activation of PI3K/AKT signaling pathway.

A Multifunctional 3D Supermolecular Co Coordination Polymer With Potential for CO2 Adsorption, Antibacterial Activity, and Selective Sensing of Fe3+/Cr3+ Ions and TNP.

A 3D supermolecular structure [Co3(L)2 (2,2'-bipy)2](DMF)3(H2O)3 1) (H3L = 4,4',4″-nitrilotribenzoic acid) has been constructed based on H3L, and 2,2'-bipy ligands under solvothermal conditions. Compound 1 can be described as a (3, 6)-connected kgd topology with a Schläfli symbol (43)2(46.66.83) formed by [Co3(CO2)6] secondary building units. The adsorption properties of the activated sample 1a has been studied; the result shows that 1a has a high adsorption ability: the CO2 uptakes were 74 cm3·g-1 at 273 K, 50 cm3·g-1 at 298 K, the isosteric heat of adsorption (Qst) is 25.5 kJ mol-1 at zero loading, and the N2 adsorption at 77 K, 1 bar is 307 cm3 g-1. Magnetic measurements showed the existence of an antiferromagnetic exchange interaction in compound 1, besides compound 1 exhibits effective luminescent performance for Fe3+/Cr3+ and TNP.

Role of extracellular polymeric substances on the behavior and toxicity of silver nanoparticles and ions to green algae Chlorella vulgaris.

The effect of extracellular polymeric substances (EPS), vital organic matters and nutrient elements in the natural environment, on the behavior and toxicology of silver nanoparticles (AgNPs) and ions remains ambiguous. In this study, the role of EPS on the toxicity of AgNPs and dissolved silver ions (from AgNO3) to a green algae Chlorella vulgaris was investigated. After the removal of EPS, algae accumulated more silver, about 7.41- and 1.25-fold of those in the algae with EPS for AgNPs and AgNO3 treatments, respectively. The large amount of accumulated silver was bound to the algal cell surface for AgNPs treatment and was internalized in the algae for AgNO3 treatment, irrespective of the presence of EPS in algae. After exposure to AgNPs, the ruffles in the surfaces of algal cells were filled by AgNPs, and almost invisible. FTIR showed that for both AgNPs and AgNO3, the aldehyde groups on the cell surface were oxidized to carboxyl groups by silver ions, irrespective of the presence of EPS in algal cells, indicating that silver ions were released from the oxidization of AgNPs and reacted with algal cells. The content of chlorophyll showed that AgNPs depressed algal growth more remarkably than did AgNO3, independent of the presence of EPS in algae, suggesting that AgNPs had greater toxic effects on algae than did silver ions. The findings suggest that the barrier effect of EPS gave nanoparticles an extraordinary edge over ions, but EPS had no discerning effect on the interaction of algal cells with the silver ions released from AgNPs and AgNO3, and also on the effect of AgNPs and AgNO3 on algal growth.

Intoxication and biochemical responses of freshwater snail Bellamya aeruginosa to ethylbenzene.

No acute toxic data of ethylbenzene on gastropod is available in literature. In the present study, the acute toxicity of ethylbenzene was assessed on a freshwater snail Bellamya aeruginosa, which was exposed to ethylbenzene concentration from 1 to 100 mg/L for 96 h. No mortality occurred, but a manifestation of intoxication (distress syndrome) was observed in part of exposed snails, and meanwhile, another part was moved normally. The distress syndrome showed clear dose- and time-dependent effects, and the 96-h EC50 value for distress syndrome was 13.3 mg/L in snail. The biochemical responses induced by ethylbenzene to the snail, including acetylcholinesterase (AChE) in the whole body and superoxide dismutase (SOD), catalase (CAT), glutathione S-transferases (GST), and reduced glutathione (GSH) in the hepatopancreas, were evaluated both for distressed snail and moved snail. The AChE activity of distressed snail was all inhibited more than 45 %, and the inhibition of AChE activity in the moved snail was all less than 30 % and more than 20 %, demonstrating that ethylbenzene exerted nervous toxicity to both distressed snail and moved snail. Meanwhile, the difference for AChE activity between the two different response snails was significant. Among the antioxidant biomarkers (SOD, CAT, GST, and GSH), only GST displayed significant difference between the distressed snail and moved snail. However, the activities of enzymes (SOD, CAT, and GST) in the moved snail were greater than those in the distressed snail, no matter significantly or insignificantly, which indicated that the ability of antioxidant defense in the distressed snail was weaker than that in the moved snail. The findings here reported manifest that ethylbenzene exerted nervous toxicity to snail, and the snail with intoxication response (distress syndrome) presented larger inhibition on AChE activity and weaker antioxidant ability in comparison with the moved snail.

Responses of oxidative stress biomarkers and DNA damage on a freshwater snail (Bellamya aeruginosa) stressed by ethylbenzene.

Ethylbenzene is classified as a priority pollutant; however, toxicity data, especially those regarding sublethal toxicity, are rarely reported on gastropods. The present work was performed to elucidate the sublethal effects of ethylbenzene using a freshwater snail, Bellamya aeruginosa (Reeve), exposed to ethylbenzene for 21 days followed by a 17-day recovery period. Superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), reduced glutathione (GSH), and malonyldialdehyde (MDA) were used as biomarkers to evaluate oxidative stress in hepatopancreas of snails. In addition, alkaline comet assay was applied to determine the genotoxicity of ethylbenzene in hepatopancreas of snails. These biomarkers and DNA damage exhibited various responses to ethylbenzene in the tested snails. SOD and CAT activities were almost significantly stimulated during the exposure period. As exposure time was prolonged beyond 7 days, CAT activity gradually became significantly increased at higher doses of ethylbenzene. GSH concentration was positively and linearly related with exposure dose. MDA concentration was significantly greater than that in the control only under the lowest treatment after a 7-day exposure. Alkaline comet assay showed that ethylbenzene could significantly induce DNA damage in hepatopancreas of snails, and there was a good dose- and time-response in DNA damage, indicating potential genotoxicity of ethylbenzene on snails. At the end of the recovery period, the repair of DNA damage was not yet completed, showing that DNA repair requires more time. The findings from this study could indicate that SOD, GST, and GSH seem to be effective oxidative biomarkers for snails exposed to ethylbenzene in the short term. CAT proved to be a valuable discriminating biomarker in subchronic exposure to ethylbenzene, but MDA was not a suitable oxidative biomarker for exposure to ethylbenzene in either the short or long term. Alkaline comet assay was efficient tool with which to evaluate the potential genotoxicity of ethylbenzene.

Behavioral alteration and DNA damage of freshwater snail Bellamya aeruginosa stressed by ethylbenzene and its tissue residue.

To study the sublethal effects induced by ethylbenzene and the capability of a freshwater gastropod Bellamya aeruginosa to take up and depurate ethylbenzene, the snail was subjected to two treatments, a 23-day exposure period followed by a 17-day depuration period. Behavioral alteration, namely retraction response, was observed during the exposure period, and the proportion of retracted snails increased under each treatment as the exposure time prolonged but there was no linear relationship between the retracted proportion and the exposure dose. Such behavioral alteration was probably due to the disturbance of membrane permeability stressed by ethylbenzene. Ethylbenzene uptake in unretracted snails was greater than in retracted snails, while the depuration abilities in the two different responses of snails had no significant difference from each other. Because of the limited capability of snails to detoxify ethylbenzene, the depuration was mainly through a slow excretion process and therefore ethylbenzene was still present in the tissue of snail after 17-day depuration. DNA damage was induced significantly in snails exposed to ethylbenzene, and the levels of DNA damage showed positive time-response and dose-response relationships, and moreover the levels of DNA damage had no difference between the two different responses of snails. There was no linear relationship between the level of DNA damage and the amount of residual ethylbenzene in tissue, which may be related to the adaptation mechanism in snail. Overall, the results suggest that the snail has high capability to take up ethylbenzene and low ability to depurate it, and ethylbenzene has potential genotoxicity to snail.