77 research outputs found
Hydrogen Bonding Paradigm in the Formation of Crystalline KH<sub>2</sub>PO<sub>4</sub> from Aqueous Solution
Revealing
the hydrogen bonding paradigm is critical to clarify
the formation mechanism of hydrogen bonded materials. The nucleation
process of a typical nonlinear optical crystal, KH<sub>2</sub>PO<sub>4</sub>, is identified by in situ molecular vibration spectroscopy,
which effectively demonstrates the oriented role of hydrogen bonding
in local structure engineering. On the basis of the vibrational evolution
of hydrogen bonds, the partition of different periods in the formation
of crystalline KH<sub>2</sub>PO<sub>4</sub> from aqueous solution
becomes clear. In KH<sub>2</sub>PO<sub>4</sub> aqueous solution, there
are hydrated status, (H<sub>2</sub>PO<sub>4</sub><sup>–</sup>)<sub><i>n</i></sub> aggregations, and prenucleation clusters.
The prenucleation clusters exist in the solution with a metastable
status over a period of time, and then they will transform into crystalline
ones within a short time. Two distinct roles of P–O···H–O–P
hydrogen bonding in the formation of crystalline KH<sub>2</sub>PO<sub>4</sub> have been distinguished. At the initial stage of aggregation
formation, P–O bond in H<sub>2</sub>PO<sub>4</sub><sup>–</sup> group guides the P–O···H–O–P
hydrogen bonding, leading to the H<sub>2</sub>PO<sub>4</sub><sup>–</sup> that retains <i>C</i><sub>2<i>v</i></sub> symmetry,
whereas P–O···H–O–P hydrogen bonding
guides the twist and rotation of H<sub>2</sub>PO<sub>4</sub><sup>–</sup> groups in prenucleation clusters, promoting the local structural
evolution of (H<sub>2</sub>PO<sub>4</sub><sup>–</sup>)<sub><i>n</i></sub> from <i>C</i><sub>2<i>v</i></sub> to <i>D</i><sub>2<i>d</i></sub> and the
formation of crystalline KH<sub>2</sub>PO<sub>4</sub> nuclei. The
present work deepens the hydrogen bonding effect that can warrant
much space to adjust the chemical bonding environment in constructing
crystallographic frames
Hydrogen Bonding Dependent Mesoscale Framework in Crystalline Ln(H<sub>2</sub>O)<sub>9</sub>(CF<sub>3</sub>SO<sub>3</sub>)<sub>3</sub>
Structurally,
hydrogen bonding is identified as a key factor to
domain the construction of a crystallographic frame during the crystallization
of the LnÂ(H<sub>2</sub>O)<sub>9</sub>Â(CF<sub>3</sub>SO<sub>3</sub>)<sub>3</sub> (Ln = La–Lu) system. In situ Raman spectroscopy
is used to capture the hydrogen bonding dependent mesoscale frameworks
that are formed during LnÂ(H<sub>2</sub>O)<sub>9</sub>Â(CF<sub>3</sub>SO<sub>3</sub>)<sub>3</sub> crystallization in aqueous solution
by continuously collecting the spectra of structural fragments. The
spectral characteristics show that the isolated LnÂ(H<sub>2</sub>O)<sub>9</sub><sup>3+</sup> tricapped trigonal prisms cannot exist in the
aqueous solution. With the concentration of aqueous solution, the
hydrated Ln<sup>3+</sup> and CF<sub>3</sub>SO<sub>3</sub><sup>–</sup> tend to share common H<sub>2</sub>O molecules, and new hydrogen
bonding will be built surrounding Ln<sup>3+</sup>. Especially, for
the Nd, Eu, Yb, and Lu system, LnÂ(H<sub>2</sub>O)<sub><i>n</i></sub>Â(CF<sub>3</sub>SO<sub>3</sub>)<sub>3</sub> (<i>n</i> = 8–9) clusters instead of hydrated Ln<sup>3+</sup> and CF<sub>3</sub>SO<sub>3</sub><sup>–</sup> are formed in the solution.
Under the guiding of intermolecular hydrogen bonds, both bond lengths
and bond angles of Ln–O may be regulated, leading to the initial
formation of LnÂ(H<sub>2</sub>O)<sub>6</sub><sup>3+</sup> prisms and
the following LnÂ(H<sub>2</sub>O)<sub>9</sub><sup>3+</sup> tricapped
trigonal prisms. Meanwhile, the symmetry of both CF<sub>3</sub> and
SO<sub>3</sub> groups decreases from <i>C</i><sub>3<i>h</i></sub> to <i>C</i><sub>2</sub> accompanied by
the formation of LnÂ(H<sub>2</sub>O)<sub>6</sub><sup>3+</sup> triprism.
The present study opens up the chemical bonding behaviors of rare
earth ions in aqueous solution, which provides basic data for the
study of the coordination of rare earth complexes and the design of
novel rare earth materials
A Permissive Amide <i>N</i>‑Methyltransferase for Dithiolopyrrolones
Amide N-methylation
is important for
the activity
and permeability of bioactive compounds but can be challenging to
perform selectively. The broad-spectrum antimicrobial natural products
thiolutin and holomycin differ only by an N-methyl
group at the endocyclic amide of thiolutin, but only thiolutin exhibits
antifungal activity. The enzyme responsible for amide N-methylation in thiolutin biosynthesis has remained elusive. Here,
we identified and characterized the amide N-methyltransferase
DtpM that is encoded >400 kb outside of the thiolutin gene cluster.
DtpM catalyzes efficient conversion of holomycin to thiolutin, exhibits
broad substrate scope toward dithiolopyrrolones, and has high thermal
stability. In addition, sequence similarity network analysis suggests
DtpM is more closely related to phenol O-methyltransferases
than some amide methyltransferases. This study expands the limited
examples of amide N-methyltransferases and may facilitate
chemoenzymatic synthesis of diverse dithiolopyrrolone compounds as
potential therapeutics
Chemical and Enzymatic Transformations of Nimesulide to GSH Conjugates through Reductive and Oxidative Mechanisms
Nimesulide
(NIM) is a nonsteroidal anti-inflammatory drug, and
clinical treatment with NIM has been associated with severe hepatotoxicity.
The bioactivation of nitro-reduced NIM (NIM-NH<sub>2</sub>), a major
NIM metabolite, has been thought to be responsible for the hepatotoxicity
of NIM. However, we found that NIM-NH<sub>2</sub> did not induce toxic
effects in primary rat hepatocytes. This study aimed to investigate
other bioactivation pathways of NIM and evaluate their association
with hepatotoxicity. After incubating NIM with NADPH- and GSH-supplemented
human or rat liver microsomes, we identified two types of GSH conjugates:
one was derived from the attachment of GSH to NIM-NH<sub>2</sub> (NIM-NH<sub>2</sub>-GSH) and the other one was derived from a quinone-imine intermediate
(NIM-OH-GSH). NIM-NH<sub>2</sub>-GSH was generated not only by the
oxidative activation of NIM-NH<sub>2</sub> but also from the reductive
activation of NIM. Both NADPH and GSH could act as reducing agents.
Moreover, aldehyde oxidase also participated in the reductive activation
of NIM. NIM-OH-GSH was generated mainly from NIM via epoxidation with
CYP1A2 as the main catalyzing enzyme. NIM was toxic to both primary
human and rat hepatocytes, with IC<sub>50</sub> values of 213 and
40 μM, respectively. Inhibition of the oxidative and reductive
activation of NIM by the nonspecific CYP inhibitor 1-aminobenzotriazole
and selective aldehyde oxidase inhibitor estradiol did not protect
the cells from NIM-mediated toxicity. Moreover, pretreating cells
with l-buthionine-sulfoximine (a GSH depletor) did not affect
the cytotoxicity of NIM. These results suggested that oxidative and
reductive activation of NIM did not cause the hepatotoxicity and that
the parent drug concentration was associated with the cytotoxicity
DataSheet_1_The effects of atmospheric nitrogen deposition in coral-algal phase shifts on remote coral reefs.pdf
Remote seawater has been considered a potential refuge for corals in the face of anthropogenic disturbances. However, these remote areas may receive increased atmospheric N deposition, and the ecological consequences remain unclear. This field survey revealed coral-algal phase shifts in the mid-north of the South China Sea. These shifts were observed in 44%, 13.6%, and 26.5% of the sampled reef sites at depths of 1-4Â m, 5-8Â m, and 10-15Â m, respectively. Over 50% of sections in the deeper depths hosted fewer corals compared to shallower areas, coinciding with a higher abundance of macroalgae in the deeper layers. Furthermore, based on long-term observation of atmospheric N flux, laboratory experiments were conducted to explore the cause of coral declines. The results indicate that N supply efficiently promoted macroalgae growth. The saturation of N absorption by macroalgae occurred within 2 weeks, leading to nutrient accumulation in seawater, especially nitrate, which had a direct impact on corals. While moderate N fluxes appeared to mitigate coral bleaching, high N fluxes, even with a balanced P supply or medium level of nutrients with an imbalanced N/P ratio, can both increase the susceptibility of corals to heat bleaching. This study explains the coral-algal phase shift in remote and relatively deep seawater and improves understanding of the cause-and-effect relationship between atmospheric N deposition and coral reef decline.</p
Characteristics of Cu-NPs used in this study.
<p>Transmission electron microscopy (TEM) image, scale bar = 100 nm; (B) size distribution of Cu-NPs, with measurements obtained from the TEM images.</p
Reactive oxygen species (ROS) formation (A)and oxidative stress(B-E) in the primary hepatocytes of juvenile <i>E</i>.<i>coioides</i> after CuSO<sub>4</sub> or Cu-NPs exposure.
<p>Data are means ±SD (n = 3). Significant differences (<i>p <</i>0.05) among treatments were indicated by different letters.</p
Cell viability and lactate dehydrogenase (LDH) leakage in primary hepatocytes of juvenile <i>E</i>.<i>coioides</i> after CuSO<sub>4</sub> or Cu-NPs exposure.
<p>Data are means ±SD (n = 3). Significant differences (<i>p <</i>0.05) among treatments were indicated by different letters.</p
p53 protein expression in primary hepatocytes of juvenile <i>E</i>.<i>coioides</i> after CuSO<sub>4</sub> or Cu-NPs exposure.
<p>p53 protein expression in primary hepatocytes of juvenile <i>E</i>.<i>coioides</i> after CuSO<sub>4</sub> or Cu-NPs exposure.</p
Scheme showing the proposed mechanisms of Cu-NPs and CuSO<sub>4</sub> toxicity to primary hepatocytes of <i>E</i>.<i>coioides</i>.
<p>Cu-NPs and CuSO<sub>4</sub> exhibited similar types of toxic mechanisms.</p
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