Cu2+-Citrate-Chitosan Complex Nanoparticles for the Chemodynamic Therapy of Lung Cancer.

Lung cancer poses a significant threat to human health. Surgical intervention is the preferred treatment modality for lung cancer, but a large number of patients are deprived of the opportunity for surgery for various reasons and are compelled to undergo radiotherapy and chemotherapy, which entail systemic adverse reactions. In recent years, with the advancement of nanomedicine, chemodynamic therapy (CDT) based on free radicals has been extensively investigated. In this study, we fabricated copper-citrate-chitosan composite nanoparticles (CuCC NPs) by encapsulating copper-citrate complexes with natural chitosan polymers, resulting in a substantial reduction in the biotoxicity of copper ions. The CuCC NPs selectively accumulated in tumor tissues through the enhanced permeability and retention effect (EPR) and gradually degraded within the acidic and glutathione (GSH)-rich microenvironment of the tumor, thereby releasing the loaded copper ions. Through CDT, the copper ions converted the overexpressed hydrogen peroxide (H2O2) in the tumor tissue into hydroxyl radicals (•OH), leading to the eradication of tumor cells. In animal experiments, CuCC NPs exhibited remarkable efficacy in CDT. Further histopathological and hematological analyses demonstrated that CuCC NPs could induce substantial apoptosis in tumor tissues while maintaining an extremely high level of safety.

Treated wastewater and weak removal mechanisms enhance nitrate pollution in metropolitan rivers.

The focus of urban water environment renovation has shifted to high nitrate (NO3-) load. Nitrate input and nitrogen conversion are responsible for the continuous increase in nitrate levels in urban rivers. This study utilized nitrate stable isotopes (δ15N-NO3- and δ18O-NO3-) to investigate NO3- sources and transformation processes in Suzhou Creek, located in Shanghai. The results demonstrated that NO3- was the most common form of dissolved inorganic nitrogen (DIN), accounting for 66 ± 14% of total DIN with a mean value of 1.86 ± 0.85 mg L-1. The δ15N-NO3- and δ18O-NO3- values ranged from 5.72 to 12.42‰ (mean value: 8.38 ± 1.54‰) and -5.01 to 10.39‰ (mean value: 0.58 ± 1.76‰), respectively. Based on isotopic evidence, the river received a significant amount of nitrate through direct exogenous input and sewage ammonium nitrification, while nitrate removal (denitrification) was insignificant, resulting in nitrate accumulation. Analysis using the MixSIAR model revealed that treated wastewater (68.3 ± 9.7%), soil nitrogen (15.7 ± 4.8%) and nitrogen fertilizer (15.5 ± 4.9%) were the main sources of NO3- in rivers. Despite the fact that Shanghai's urban domestic sewage recovery rate has reached 92%, reducing nitrate concentrations in treated wastewater is crucial for addressing nitrogen pollution in urban rivers. Additional efforts are needed to upgrade urban sewage treatment during low flow periods and/or in the main stream, and to control non-point sources of nitrate, such as soil nitrogen and nitrogen fertilizer, during high flow periods and/or tributaries. This research provides insights into NO3- sources and transformations, and serves as a scientific basis for controlling NO3- in urban rivers.

The contribution of wetland plant litter to soil carbon pool: Decomposition rates and priming effects.

Plant litter input is an important driver of soil/sediment organic carbon (SOC) turnover. A large number of studies have targeted litter-derived C input tracing at a global level. However, little is known about how litter carbon (C) input via various plant tissues affects SOC accumulation and mineralization. Here, we conducted laboratory incubation to investigate the effects of leaf litter and stem litter input on SOC dynamics using the natural 13C isotope technique. A 122-day laboratory incubation period showed that litter input facilitated SOC accumulation. Leaf and stem litter inputs increased soil total organic carbon content by 37.6% and 15.5%, respectively. Leaf litter input had a higher contribution to SOC accumulation than stem litter input. Throughout the incubation period, the δ13C values of stem litter and leaf litter increased by 1.5‰ and 3.3‰, respectively, while δ13CO2 derived from stem litter and δ13CO2 derived from leaf litter decreased by 4.2‰ and 6.1‰, respectively, suggesting that the magnitude of δ13C in litter and δ13CO2 shifts varied, depending on litter tissues. The cumulative CO2-C emissions of leaf litter input treatments were 27.56%-42.47% higher than those of the stem litter input treatments, and thus leaf litter input promoted SOC mineralization more than stem litter input. Moreover, the proportion of increased CO2-C emissions to cumulative CO2-C emissions (57.18%-92.12%) was greater than the proportion of litter C input to total C (18.7%-36.8%), indicating that litter input could stimulate native SOC mineralization, which offsets litter-derived C in the soil. Overall, litter input caused a net increase in SOC accumulation, but it also accelerated the loss of native SOC. These findings provide a reliable basis for assessing SOC stability and net C sink capacity in wetlands.

Bay41-4109-induced aberrant polymers of hepatitis b capsid proteins are removed via STUB1-promoted p62-mediated macroautophagy.

The hepatitis B virus (HBV) core protein (HBc) functions in multiple steps of the viral life cycle. Heteroaryldihydropyrimidine compounds (HAPs) such as Bay41-4109 are capsid protein allosteric modulators that accelerate HBc degradation and inhibit the virion secretion of HBV, specifically by misleading HBc assembly into aberrant non-capsid polymers. However, the subsequent cellular fates of these HAP-induced aberrant non-capsid polymers are not well understood. Here, we discovered that that the chaperone-binding E3 ubiquitin ligase protein STUB1 is required for the removal of Bay41-4109-induced aberrant non-capsid polymers from HepAD38 cells. Specifically, STUB1 recruits BAG3 to transport Bay41-4109-induced aberrant non-capsid polymers to the perinuclear region of cells, thereby initiating p62-mediated macroautophagy and lysosomal degradation. We also demonstrate that elevating the STUB1 level enhances the inhibitory effect of Bay41-4109 on the production of HBeAg and HBV virions in HepAD38 cells, in HBV-infected HepG2-NTCP cells, and in HBV transgenic mice. STUB1 overexpression also facilitates the inhibition of Bay41-4109 on the cccDNA formation in de novo infection of HBV. Understanding these molecular details paves the way for applying HAPs as a potentially curative regimen (or a component of a combination treatment) for eradicating HBV from hepatocytes of chronic infection patients.

Proton-coupled electron transfer of catechin in tea wine: the enhanced mechanism of anti-oxidative capacity.

Tea wine is a Chinese traditional alcoholic drink made by cereal and tea leaves. It is rich in tea polyphenols, caffeine, amino acids, and protons and possesses various healthcare functions. In this work, electrochemical methods, as well as density functional theory (DFT) calculations, were adopted to reveal the proton-coupled electron-transfer process of catechin in tea wine. The electrochemical results showed that the catechin preferred hydrogen-bonding with ethanol and formed molecular clusters. Thus, the direct electron-transfer process of catechin changed to proton-coupled electron transfer. This procedure reduced the energy barrier of the redox reaction and enhanced the anti-oxidative capacity. Subsequently, DFT calculations were employed to explore the bond length, bond energy, and HOMO-LUMO energy gap of catechin, which confirmed the above-mentioned mechanism. Our work offers some positive value for the scientific promotion of traditional food and a greater understanding of the health mechanisms in terms of chemistry.