Search

Silver nanoparticles (AgNPs) are the most commonly used engineered nanomaterials in commercialized products because of their antimicrobial activity. Previously, we have shown that polyvinylpyrrolidone (PVP)-coated AgNPs have an anti-leukemia effect against human myeloid leukemia cells; however, whether AgNPs are able to trigger autophagy in normal hematopoietic cells and the role of autophagy in AgNP-induced cytotoxicity remain unclear. In the current study, we observed that AgNPs were taken up by murine pro-B cells (Ba/F3), and then promoted accumulation of autophagosomes, which resulted from the induction of autophagy rather than the blockade of autophagic flux. AgNPs induced cytotoxicity in a dose-dependent manner accompanied by apoptosis and DNA damage through the production of reactive oxygen species (ROS) and the release of silver ions. The ROS-mediated mTOR signaling pathway was responsible for the induction of autophagy. More importantly, the inhibition of autophagy with the addition of 3-methyladenine (3-MA) or silencing of Atg5 significantly attenuated the cytotoxicity of AgNPs in Ba/F3. These findings suggest that autophagy is involved in the cytotoxicity of PVP-coated AgNPs in normal hematopoietic cells, and the inhibition of autophagy is a novel and potent strategy to protect normal hematopoietic cells upon treatment with AgNPs.

The cytotoxicity of micro/nanoplastics (MNPs) is known to be strongly influenced by particle size, but the mechanism is not clear so far. We reported the ability of polystyrene MNPs to be internalized by HeLa cells could be a reason for the size dependent cytotoxicity of MNPs. We found that small MNPs (10 nm and 15 nm in radius) could be efficiently internalized by HeLa cells, MNPs of 25 nm in radius could be slightly internalized by the cells, and larger MNPs could not enter the cells at all. We showed that only MNPs, which could be internalized by cells, had a toxic effect on cell activity in a dose-dependent manner. In contrast, MNPs, which could not be internalized by cells, showed no cytotoxicity even if at extremely high concentrations. We attributed the correlation between the size-dependent uptake of MNPs and the size-dependent cytotoxicity of MNPs to the enhanced reactive oxygen species (ROS) level and abnormal gene expression. Our study pointed out that cellular uptake is one of the most fundamental mechanisms for the cytotoxicity of MNPs. [ABSTRACT FROM AUTHOR]

2,2-bis(chloromethyl) trimethylene bis[bis(2-chloroethyl) phosphate] (V6) has been widely used as an additive in a variety of plastics due to its extremely low toxicity. However, we showed in the study that once mixed with nanopolystyrene particles (NPs), the nontoxic V6 could exhibit significant toxicity to HeLa cells. The enhanced toxicity was much higher than the toxicity of NPs alone and was related to the size of NPs. The mixture of V6 and small polystyrene NPs (10 nm and 15 nm in radius) showed obvious toxicity to HeLa cells. The toxicity increased with the concentrations of both V6 and NPs. On the contrary, the mixture of V6 and larger NPs (25 nm, 50 nm, 100 nm, and 500 nm in radius) showed almost no toxicity even at extremely high concentrations (NPs: 100 mg/L; V6: 50 mg/L). The small NPs could enter the cells and accumulated in cytoplasm. However, the larger NPs did not distribute inside the cells. NPs efficiently adsorbed V6 on the surface. The mechanism of the enhanced toxicity was attributed to the increased intracellular reactive oxygen species (ROS) production and the regulation of gene expression concerning apoptosis and ROS scavenging. Our study not only showed that a safe chemical V6 could be turned to be toxic by NPs, but also pointed out a potential risk caused by the joint toxicity of 'safe' chemicals and plastic particles with small size. [ABSTRACT FROM AUTHOR]

Simple Summary: Early leaf senescence is an important agronomic trait that affects crop yield and quality. To understand the molecular mechanism of early leaf senescence, a wheat (Triticum aestivum L.) premature leaf senescence mutant (GSm) and its wild type were employed in this study. We compared the physiological characteristics and transcriptome of wheat leaves between the wild type (WT) and the mutant at two-time points. Physiological characteristics and differentially expressed gene (DEG) analysis revealed many genes and metabolic pathways that were closely related to senescence. These results will not only support further gene cloning and functional analysis of GSm, but also facilitate the study of leaf senescence in wheat. Premature leaf senescence has a profound influence on crop yield and quality. Here, a stable premature senescence mutant (GSm) was obtained from the common wheat (Triticum aestivum L.) cultivar Chang 6878 by mutagenesis with ethyl methanesulfonate. The differences between the GSm mutant and its wild-type (WT) were analyzed in terms of yield characteristics, photosynthetic fluorescence indices, and senescence-related physiological parameters. RNA sequencing was used to reveal gene expression differences between GSm and WT. The results showed that the yield of GSm was considerably lower than that of WT. The net photosynthetic rate, transpiration rate, maximum quantum yield, non-photochemical quenching coefficient, photosynthetic electron transport rate, soluble protein, peroxidase activity, and catalase activity all remarkably decreased in flag leaves of GSm, whereas malondialdehyde content distinctively increased compared with those of WT. The analysis of differentially expressed genes indicated blockade of chlorophyll and carotenoid biosynthesis, accelerated degradation of chlorophyll, and diminished photosynthetic capacity in mutant leaves; brassinolide might facilitate chlorophyll breakdown and consequently accelerate leaf senescence. NAC genes positively regulated the senescence process. Compared with NAC genes, expression of WRKY and MYB genes was induced earlier in the mutant possibly due to increased levels of reactive oxygen species and plant hormones (e.g., brassinolide, salicylic acid, and jasmonic acid), thereby accelerating leaf senescence. Furthermore, the antioxidant system played a role in minimizing oxidative damage in the mutant. These results provides novel insight into the molecular mechanisms of premature leaf senescence in crops. [ABSTRACT FROM AUTHOR]

Apoptin is a protein that specifically induces apoptosis in tumor cells. The anti-tumorigenic functions of Apoptin, including autophagy activation and its interaction with apoptosis, have not been precisely elucidated. Here we investigate the main pathways of apoptin-mediated killing of human liver cancer cells, as well as its putative role in autophagy and apoptosis. The anti-proliferative effect of apoptin in liver cancer cells was analyzed in vitro by crystal violet staining and MTS detection, and also in vivo using a tumor-based model. The main pathway related to apoptin-induced growth inhibition in vitro was evaluated by flow cytometry and fluorescence staining. The relationship between apoptosis and autophagy on apoptin-treating cells was analyzed using apoptosis and autophagy inhibitors, mitochondrial staining, Annexin V-FITC/PI flow detection, LC3 staining, and western blotting. The effect of ROS toward the apoptosis and autophagy of apoptin-treating cells was also evaluated by ROS detection, Annexin V-FITC/PI flow detection, LC3 staining, and western blotting. Inhibition of apoptosis in apoptin-treating liver cancer cells significantly reduced the autophagy levels in vitro. The overall inhibition increased from 12 h and the effect was most obvious at 48 h. Inhibition of autophagy could increase apoptin-induced apoptosis of cells in a time-dependent manner, reaching its peak at 24 h. Apoptin significantly alters ROS levels in liver cancer cells, and this effect is directly related to apoptosis and autophagy. ROS appears to be the key factor linking apoptin-induced autophagy and apoptosis through the mitochondria in liver cancer cells. Therefore, evaluating the interaction between apoptin-induced apoptosis and autophagy is a promising step for the development of alternate tumor therapies. [ABSTRACT FROM AUTHOR]

Glucose-6-phosphate dehydrogenase (G6PDH or G6PD) is the key regulatory enzyme in the oxidative pentose phosphate pathway (OPPP). The cytosolic isoforms including G6PD5 and G6PD6 account for the major part of the G6PD total activity in plant cells. Here, we characterized the Arabidopsis single null mutant g6pd5 and g6pd6 and double mutant g6pd5/6. Compared to wild type, the mutant seeds showed a reduced germination rate and root elongation under salt stress. The seeds and seedlings lacking G6PD5 and G6PD6 accumulate more reactive oxygen species (ROS) than the wild type under salt stress. Cytosolic G6PD (cy-G6PD) affected the expression of NADPH oxidases and the G6PD enzymatic activities in the mutant atrbohD/F , in which the NADPH oxidases genes are disrupted by T-DNA insertion and generation of ROS is inhibited, were lower than that in the wild type. The NADPH level in mutants was decreased under salt stress. In addition, we found that G6PD5 and G6PD6 affected the activities and transcript levels of various antioxidant enzymes in response to salt stress, especially the ascorbate peroxidase and glutathione reductase. Exogenous application of ascorbate acid and glutathione rescued the seed and root phenotype of g6pd5/6 under salt stress. Interestingly, the cytosolic G6PD negatively modulated the NaCl-blocked primary root growth under salt stress in the root meristem and elongation zone. [ABSTRACT FROM AUTHOR]

• Spraying EBR at 5μmol L−1 was optimal in inhibiting the decay of strawberries. • EBR inhibited the increase of bitterness and the decrease of sweetness of berries. • EBR increased the contents of amyl acetate-D and butanoic acid ethyl ester. • EBR activated ROS metabolism by inducing genes expression of ROS scavenging enzymes. • Spraying EBR enhanced the antioxidant capacity of strawberries. The effects of exogenous 2,4-Epibrassinolide (EBR) on the sensory quality and antioxidant capacity of postharvest strawberries were evaluated. Strawberries were sprayed with varying concentrations of EBR (0, 1, 2.5, 5, 10 μmol L−1) and stored at 20 °C for 5 d. This finding revealed that EBR at 5 μmol L−1 proved to be the most effective in maintaining the quality characteristics and delaying the decay of postharvest strawberries. The treatment of EBR at 5 μmol L−1 repressed the increase of bitterness and inhibited the decline in sweetness and firmness, without causing detrimental impact on total soluble solids (TSS) and texture of strawberries. Additionally, EBR at 5 μmol L−1 had a positive impact on strawberry aroma and promoted the accumulation of butanoic acid, methyl ester, ethyl 3-acetylpropionate-M and 2- heptanone-D. It also enhanced the activities of superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) by activating the gene expression of FaMnSOD, FaCu/ZnSOD, FaCAT and FaAPX , and thus inhibited the accumulation of hydrogen peroxide (H 2 O 2) and superoxide radical anions (O 2 ·−). The activation of ROS metabolism led to the higher antioxidant capacity compared with control. The findings suggested that EBR treatment was promising in improving the sensory characteristics and enhancing the antioxidant capacity of postharvest strawberries. [Display omitted] [ABSTRACT FROM AUTHOR]

The electronic structure and optical properties of MoS 2 /SnO 2 hetero-bilayer have been systematically investigated with hybrid functional calculations. The band dispersion character of monolayer MoS 2 at the VBM and that of monolayer SnO 2 at CBM are well preserved in the MoS 2 /SnO 2 hetero-bilayer, and thus the effective separation of electrons and holes is expected. Besides, the band gap narrowing in the MoS 2 /SnO 2 hetero-bilayer can accordingly enhance the effective utilization of the solar spectrum, especially in the visible light region. Additionally, the MoS 2 /SnO 2 hetero-bilayer that is active for both the photo-oxidation and photo-reduction of water possesses superior photocatalytic activity than that of monolayer MoS 2 and SnO 2. Image 1073 • The monolayer MoS 2 can grow on the monolayer SnO 2 substrate. • Electron and hole with high-mobility can be separated in MoS 2 /SnO 2 hetero-bilayer. • The MoS 2 /SnO 2 hetero-bilayer enhances the effective utilization of visible light. • A red shift of absorption edge could occur in MoS 2 /SnO 2 hetero-bilayer. • The MoS 2 /SnO 2 hetero-bilayer is active for both the oxygen and hydrogen evolution. [ABSTRACT FROM AUTHOR]

Recently micro/nanoplastics (MNPs) have raised intensive concerns due to their possible enhancement effect on the dissemination of antibiotic genes. Unfortunately, data is still lacking to verify the effect. In the study, the influence of polystyrene MNPs on the conjugative gene transfer was studied by using E. coli DH5ɑ with RP4 plasmid as the donor bacteria and E. coli K12 MG1655 as the recipient bacteria. We found that influence of MNPs on gene transfer was size-dependent. Small MNPs (10 nm in radius) caused an increase and then a decrease in gene transfer efficiency with their concentration increasing. Moderate-sized MNPs (50 nm in radius) caused an increase in gene transfer efficiency. Large MNPs (500 nm in radius) had almost no influence on gene transfer. The gene transfer could be further enhanced by optimizing mating time and mating ratio. Scavenging reactive oxygen species (ROS) production did not affect the cell membrane permeability, indicating that the increase in cell membrane permeability was not related to ROS production. The mechanism of the enhanced gene transfer efficiency was attributed to a combined effect of the increased ROS production and the increased cell membrane permeability, which ultimately regulated the expression of corresponding genes. [Display omitted] • The enhancement effect of micro/nanoplastics on gene transfer was size-dependent. • The mechanism was attributed to ROS production and cell membrane permeability. • The gene transfer was further enhanced by mating time and mating ratio. • The increase in cell membrane permeability was not related to ROS production. [ABSTRACT FROM AUTHOR]

[Display omitted] • Light irradiation can significantly increase the fluorescence signal of DCFH-DA via chain reactions. • At the beginning stage, the ratio of fluorescence densities between samples keeps unchanged after light irradiation. • A more stable and sensitive ROS detection method was developed by light irradiation. • This method can not only quantitatively compare relative ROS levels between samples, but also detect extremely weak ROS. Dichlorodihydrofluorescein diacetate (DCFH-DA) has been widely used in detection of reactive oxygen species (ROS). Unfortunately, the detection process is easily affected by light irradiation during measurement, which cannot be overlooked especially for samples with a small amount of ROS. In the study, we revealed several factors that influence the ROS detection process and developed a new ROS detection method by DCFH-DA with higher stability and sensitivity. After light irradiation, the fluorescence signal of DCFH-DA solution increased significantly with pH value higher than 7.4. The increase of fluorescence signal was attributed to a self-oxidization process of DCFH-DA, which transferred dichlorodihydrofluorescein (DCFH) to 2′,7′-dichlorofluorescein (DCF) with the presence of DCF. At the beginning stage of light irradiation, i.e., when the amount of DCF was negligible compared to DCFH (DCFH-DA), the ratio of fluorescence density between samples keeps unchanged after light irradiation. On this basis, we developed a stable and sensitive ROS detection method via light irradiation. The method was successfully applied to detect ROS in HeLa cells which was induced by hydrogen peroxide (H 2 O 2) and plastic nanoparticles. A new insight into the proportional increase of fluorescence signal by light irradiation was revealed. [ABSTRACT FROM AUTHOR]