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Zinc (Zn) is a fundamental trace element for cell viability and physiology, and concentrations above the physiological level may lead to cell damage. In order to explore the effect of zinc chloride (ZnCl 2 ) on murine photoreceptor cells, in this study, we investigated the alterations of murine photoreceptor cell proliferation and cell morphology after exposure to various concentrations of ZnCl 2 , determined the levels of hydrogen peroxide, hydroxyl radicals, cytochrome c, and ATP before and after cells exposure to different concentrations of ZnCl 2 , monitored the changes of mitochondrial membrane potential, and further explored the expressions of BCL2-associated X (Bax) and B cell CLL/lymphoma (Bcl)-2 at gene and protein levels. The results indicated that appropriate ZnCl 2 levels can enhance the cell proliferation, whereas high levels of ZnCl 2 could apparently inhibit cell growth, exaggerate the generation of both hydrogen peroxide and hydroxyl radicals, collapse the mitochondrial membrane potential, and accelerate cytochrome c release into cytosol, decrease the ATP production, elevate the Bax production, and reduce the Bcl-2 expression, thereby disrupting the mitochondrial homeostasis. Consequently, the disrupted mitochondrial homeostasis initiates the mitochondria-mediated apoptotic signaling pathway, leading to cell death. Taken together, the results suggest that the over generation of reactive oxygen species and the activated mitochondrial signaling pathway play an important role in ZnCl 2 -induced murine photoreceptor cell death., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Estrogen receptors play critical roles in regulating genes responsible for development and maintenance of reproductive tissues and other physiological function. The interaction of ERs with DNA sequences, known as estrogen response elements (EREs) (a palindromic repeat separated by three-base spacer, 5'GGTCAnnnTGACC-3'), is required for estrogen regulation of target gene expression. Here, we describe a simple "mix-and-measure"-based method for detecting ER:ERE interactions using ERE-immobilized metal nanoparticles and water-soluble conjugated polyelectrolytes (CPEs) as cooperative sensing elements. This method can differentiate the distinct DNA-binding affinity between ERα and ERβ, and determine ER:ERE-binding stoichiometry. This method can also accurately detect all 15 singly mutated EREs (i.e., three possible base substitutions at each of one to five positions from left to right of the 5' end half site, GGTCA) for their binding energy to ER. This method is compatible with 96-well plate format for high-throughput analysis.

An experiment was conducted using a total of 840, 1-day-old, Arbor Acres commercial male broilers to compare copper (Cu) sulfate and tribasic Cu chloride (TBCC, Cu(2)(OH)(3)Cl) as sources of supplemental Cu for broilers fed in floor pens. Chicks were randomly allotted to one of seven treatments for six replicate pens of 20 birds each, and were fed a basal corn-soybean meal diet (10.20 mg/kg Cu) supplemented with 0, 100, 150, or 200 mg/kg Cu from either Cu sulfate or TBCC for 21 days. Chicks fed 200 mg/kg Cu as TBCC had a higher (P < 0.05) average daily gain (ADG) than those consuming other diets. Liver Cu contents of broilers fed diets supplemented with TBCC were numerically lower (P > 0.05) than those of broilers fed diets supplemented with Cu sulfate. The vitamin E contents and the phytase activities in the feed fortified with TBCC were higher (P < 0.01) and numerically higher (P > 0.05) compared with those in the feeds fortified with Cu sulfate stored at room temperature, respectively. The vitamin E contents in liver and plasma of broilers fed diets supplemented with TBCC were higher (P < 0.05) than those of birds fed diets supplemented with Cu sulfate. This result indicates that TBCC is more effective than Cu sulfate in improving the growth of broilers fed in floor pens, and it is chemically less active than Cu sulfate in promoting the undesirable oxidation of vitamin E in feeds.

Overexposure to manganese is known to cause damage to basal ganglial neurons and the development of movement abnormalities. Activation of microglia and astrocytes has increasingly been associated with the pathogenesis of a variety of neurological disorders. We have recently shown that microglial activation facilitates manganese chloride (MnCl2, 10-300 microM)-induced preferential degeneration of dopamine (DA) neurons. In this study, we report that combinations of MnCl2 (1-30 microM) and endotoxin lipopolysaccharide (LPS, 0.5-2 ng/mL), at minimally effective concentrations when used alone, induced synergistic and preferential damage to DA neurons in rat primary neuron-glia cultures. Mechanistically, MnCl2 significantly potentiated LPS-induced release of tumor necrosis factor-alpha and interleukin-1 beta in microglia, but not in astroglia. MnCl2 and LPS were more effective in inducing the formation of reactive oxygen species and nitric oxide in microglia than in astroglia. Furthermore, MnCl2 and LPS-induced free radical generation, cytokine release, and DA neurotoxicity was significantly attenuated by pre-treatment with potential anti-inflammatory agents minocycline and naloxone. These results demonstrate that the combination of manganese overexposure and neuroinflammation is preferentially deleterious to DA neurons. Moreover, these findings not only shed light on the understanding of manganese neurotoxicity but may also bear relevance to the potentially multifactorial etiology of Parkinson's disease.

Exposure to elevated levels of manganese has been shown to cause neuronal damage in the midbrain and the development of Parkinsonian symptoms. Activation of microglia and release of neurotoxic factors in particular free radicals are known to contribute to neurodegeneration. We have recently reported that manganese chloride (MnCl(2)) stimulates microglia to produce reactive oxygen species (ROS). The aim of this study is to determine the role of microglia in the MnCl(2)-induced degeneration of dopaminergic (DA) neurons that are particularly vulnerable to oxidative insult. MnCl(2) (10-300 microM; 7 days) was markedly more effective in damaging DA neurons in the rat mesencephalic neuron-glia cultures than the neuron-enriched (microglia-depleted) cultures. In addition, the microglia-enhanced MnCl(2) toxicity was found to be preferential to DA neurons. The microglial enhancement of DA neurotoxicity was further supported by the observation that replenishment of microglia to the neuron-enriched cultures significantly increased the susceptibility of DA neurons to the MnCl(2)-induced damage. Analysis of the temporal relationship between microglial activation and DA neurodegeneration revealed that MnCl(2)-stimulated microglial activation preceded DA neurodegeneration. Mechanistically, MnCl(2) (10-300 microM) stimulated a concentration- and time-dependent robust production of ROS and moderate production of nitric oxide but no detectable release of tumor necrosis factor-alpha and interleukin-1beta. Application of free radical scavengers including superoxide dismutase/catalase, glutathione, N-acetyl cysteine and an inhibitor of nitric oxide biosynthesis significantly protected DA neurons against the MnCl(2)-induced degeneration. These results demonstrate that microglial activation and the production of reactive nitrogen and oxygen free radicals promote the MnCl(2)-induced DA neurodegeneration.

Elevated exposure to manganese is known to cause neurodegeneration in the basal ganglia and to induce movement abnormalities called manganism. However, the underlying mechanism of action is not fully understood. Activation of the resident immune cells in the brain, microglia that release a variety of neurotoxic factors, has been implicated to contribute to neurodegeneration. Of the various neurotoxic factors released by activated microglia, reactive oxygen species such as superoxide and hydrogen peroxide are particularly detrimental to the survival of the oxidative damage-prone neurons. In this study, we report that exposure of rat microglia to manganese chloride (MnCl(2)) resulted in a time- and concentration-dependent release of hydrogen peroxide (H(2)O(2)). The MnCl(2)-stimulated microglial H(2)O(2) release was sensitive to inhibitors of mitogen-activated protein kinases (MAPK) but not that of NADPH oxidase. MnCl(2)-induced a rapid activation of the extracellular signal-regulated kinase (ERK) and p38-MAPK in microglia that appeared to precede the MnCl(2)-induced H(2)O(2) release, suggesting that ERK and p38-MAPK influenced the MnCl(2)-induced H(2)O(2) release in microglia. In summary, these results demonstrate that manganese chloride is capable of activating microglia to release ROS and MAPK may, in part, be key regulators of the process. These findings may shed significant light on the potential role of microglia in the manganese-induced neurotoxicity.

The reaction of chromium(III) chloride, salicylic acid (SA) and ethylenediamine (en) led to the formation of chromium complex [Cr(SA)(en)(2)]Clx2H(2)O(1). The crystal structure belongs to monoclinic system with the space group P2(1), R(1)=0.0358. In this compound, Cr(III) atom is six-coordinated in octahedral coordination geometry by one phenolic hydroxyl oxygen, one carboxylate oxygen from the salicylic acid and four nitrogen atoms from two ethylenediamine molecules, respectively. The transfer manners of Cr(III) from the title compound to the low-molecular-mass chelator, ethylenediamine-N,N,N',N'-tetraacetic acid (EDTA) and the iron-binding protein apoovotransferrin (apoOTf) were followed by a combination of UV-visible (UV-Vis) and fluorescence spectra in 0.01M Hepes at pH 7.4. The results show that Cr(III) can be transferred from the complex to apoovotransferrin with the retention of the salicylate acted as a synergistic anion.

C40H48Cl2N4O9, monoclinic, C2 (no. 5), a = 13.434(2) Å, b = 7.2089(11) Å, c = 20.691(3) Å, β = 95.931(4)°, V = 1993.0(5) Å3, Z = 2, Rgt(F) = 0.0478, wRref (F2) = 0.1091, T = 173 K. [ABSTRACT FROM AUTHOR]

The unbalanced crosstalk between osteoclasts and osteoblasts could lead to disruptive bone homeostasis. Herein, we investigated the therapeutic effects of rubidium chloride (RbCl) on ovariectomized (OVX) and titanium (Ti) particle-induced calvaria osteolysis mouse models, showing that non-toxic RbCl attenuated RANKL-stimulated osteoclast formation and functionality while significantly enhancing osteogenesis in vitro. The expressions of osteoclast-specific genes were downregulated considerably by RbCl. Despite the direct inhibition of RANKL-induced activation of MAPK signaling, RbCl was able to target NF-κB directly and indirectly. We found that after the co-stimulation of the c-Jun N-terminal kinase (Jnk)/p38 activator and RANKL, RbCl inhibited the elevated expression of p-IKKα and the degradation of IκBα in osteoclast precursors, indicating indirect NF-κB inhibition via MAPK suppression. Furthermore, the two animal models demonstrated that RbCl attenuated tartrate-resistant acid phosphate (TRAP)-positive osteoclastogenesis and rescued bone loss caused by the hormonal dysfunction and wear particle in vivo. Altogether, these findings suggest that RbCl can target Jnk/p38-mediated NF-κB activation to attenuate osteoclastogenesis, while facilitating osteoblastogenesis both in vivo and in vitro , suggesting the possible future use of RbCl for surface coating of orthopedic implant biomaterials to protect against osteoporosis. [ABSTRACT FROM AUTHOR]

Abstract: Monodisperse NiO octahedrons have been synthesized by heating NiCl2 solutions on the Si substrates at 400–500°C for 1h. The NiO octahedrons are single-crystalline with the body-centered cubic structure and have controllable sizes in the range of 166–257nm. Control over the size of NiO octahedrons was achieved by adjusting the heating temperature. The formation of NiO octahedrons results from the selective adsorption of Cl– ions on unsaturated Ni(II) sites of NiO (111) surface. The NiO octahedrons with exposed {111} facets show higher intrinsic photocatalytic activity than Degussa P25 TiO2, and the photocatalytic activity was enhanced with a decrease on the size of NiO octahedrons. [Copyright &y& Elsevier]

The interaction between dioxopromethazine hydrochloride (DPZ) and human serum albumin (HSA), in vitro, was investigated by means of fluorescence, absorption and circular dichroism (CD) spectroscopy. The results obtained from analysis of the fluorescence spectra indicate that DPZ has a strong ability to quench the intrinsic fluorescence of HSA through a static quenching mechanism. The HSA-DPZ binding distance was determined to be less than 7 nm, suggesting that energy transfer from HSA to DPZ may occur. The thermodynamic parameters of the interaction between DPZ and HSA were measured according to the van't Hoff equation. The negative enthalpy change (Δ H) and positive entropy change (Δ S) values indicate that hydrophobic and electrostatic interactions play major roles in the binding between DPZ and HSA. The binding process was a favorable process in which the Gibbs energy change (Δ G) is negative. The results of displacement experiments suggested that DPZ is located in site I of HSA within subdomain IIA. In addition, the results of absorption, synchronous fluorescence and CD spectra show that binding of DPZ with HSA can induce conformational changes in HSA. [ABSTRACT FROM AUTHOR]

Abstract: An efficient synthesis of 1,3,5-trisubstituted benzenes via a sequential Pd-mediated carbon–sulfur, carbon–nitrogen, and carbon–carbon bond formation reactions is reported. Selective amidation and sulfonamidation reactions are accomplished via Pd-catalyzed reactions between aryl chlorides and an acetamide or a methanesulfonamide. [Copyright &y& Elsevier]

Abstract: The dehydrogenation temperature of LiBH4 was considerably decreased to 230 °C–300 °C when it was manually mixed with FeCl2, CoCl2 and NiCl2 in a molar ratio of 2:1. Mixing LiBH4 with NiCl2 or FeCl2 led to complete hydrogen desorption from LiBH4, i.e. 18.3 wt% hydrogen was achieved with respect to the weight of LiBH4. However, the CoCl2 addition resulted in less hydrogen release due to the formation of diborane. Ball milling treatment for the mixtures of LiBH4 and these chlorides further decreased hydrogen desorption temperatures. The results indicate that LiBH4 could be effectively destabilized by the chlorides of Fe, Co and Ni. Small doping of these chlorides into LiBH4 was found to be effective in enhancing dehydrogenation kinetics of the remaining LiBH4 due to the formation of metal borides. [Copyright &y& Elsevier]

Esters can be successfully reduced to the corresponding alcohols with potassium borohydride/lithium chloride under microwave irradiation without solvent. The reactions are generally completed in 2–8 minutes, with the yields varying from 55% to 95%. [ABSTRACT FROM AUTHOR]

C40H48Cl2N4O9, monoclinic, C2 (no. 5), a = 13.434(2) Å, b = 7.2089(11) Å, c = 20.691(3) Å, β = 95.931(4)°, V = 1993.0(5) Å3, Z = 2, Rgt(F) = 0.0478, wRref (F2) = 0.1091, T = 173 K. [ABSTRACT FROM AUTHOR]