The ratio but not individual of fragile to refractory DOM affects greenhouse gases release in different trophic level lakes.

Inland shallow lakes are recognized as an important source of greenhouse gases (GHGs), and their contribution is expected to increase due to global eutrophication. The generation and release of GHGs involved multiple variables, leading to many uncertain potential factors. This study examined the emission characteristics of GHGs at the water-air interface in 12 shallow lakes categorized into four eutrophic levels in the Yangtze River basin. The average emission rates of CH4, CO2 and N2O were 1.55, 3.43, 18.13 and 30.47 mg m-2 h-1, 4.12, 14.64, 25.11 and 69.84 mg m-2 h-1, and 0.2, 0.25, 0.43 and 0.79 mg m-2 day-1 in the oligotrophic, mesotrophic, eutrophic and hypereutrophic lakes, respectively. There were significant correlations between eutrophic levels and the emission rates of CH4 and CO2 (p < 0.05). Redundancy analysis and Mantel test were conducted to further examine the key factors influencing carbon emissions from eutrophic water. It was found that the presence of algae and nutrients in the overlying water played a crucial role in the release of GHGs, indicating the importance of ecosystem productivity in the carbon budget of the lake. In order to assess the bioavailability of organic matter, a new indicator called R(P/H) was proposed. This indicator represents the ratio of protein and humus-like components, which were obtained through EEMs-PARAFAC modeling. The relationship between R(P/H) and CH4 was found to be exponential (R2 = 0.90). Additionally, R(P/H) showed a linear relationship with CO2 and N2O (R2 = 0.68, R2 = 0.75). Therefore, it is crucial to consider R(P/H) as an important factor in accurately estimating global GHG emission fluxes in the future, especially with advancements in the database.

Sources, Migration, Transformation, and Environmental Effects of Organic Carbon in Eutrophic Lakes: A Critical Review.

Organic carbon (OC) plays a leading role in the carbon cycle of lakes and is crucial to carbon balances at regional and even global scales. In eutrophic lakes, in addition to external river inputs, the decomposition of endogenous grass and algae is a major source of organic carbon. Outbreaks of algal blooms (algal eutrophication) and the rapid growth of aquatic grasses (grass eutrophication) can lead to the accumulation and decay of large amounts of algae and aquatic grass debris, which increases the intensity of the carbon cycle of lakes and greatly impacts aquatic environments and ecosystems. The structures, decomposition processes, and distribution characteristics of algae and higher aquatic plant debris in eutrophic lakes are different from mesotrophic and oligotrophic lakes. Studying their accumulation dynamics and driving mechanisms is key to further understanding lake carbon cycles and their many interdependent pathways. This paper focuses on the carbon sources, tracing technologies, migration and transformation processes, and environmental effects of OC in eutrophic lakes. Based on the existing knowledge, we further combed the literature to identify the most important knowledge gaps preventing an in-depth understanding of the processes and driving mechanisms of the organic carbon cycle in eutrophic lakes.

TRIM59 promotes steatosis and ferroptosis in non-alcoholic fatty liver disease via enhancing GPX4 ubiquitination.

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease around the world. However, no specific medicine has been approved for NAFLD treatment. Our study was conducted to explore the role and mechanism of TRIM59 in NAFLD, aiming to provide a novel target for NAFLD treatment. Here, the expression of TRIM family members was detected in 10 mild and severe NAFLD tissues as well as 10 normal tissues. TRIM59 expression was verified in 10 normal tissues and 25 mild and severe NAFLD tissues. Palmitic acid and high-fatty diet were used for the construction of NAFLD models. Oil Red O staining was used to detect the level of steatosis. The content of TNF-α, IL-6, and IL-8 was measured to reflect the level of inflammation. Lipid reactive oxygen species was estimated by flow cytometry. We found that TRIM59 was highly expressed in NAFLD tissues compared with normal liver tissues. The inhibition of TRIM59 could inhibit the steatosis and inflammation in NAFLD, whereas its overexpression exhibited reversed effects. The application of ferroptosis inhibitor, deferoxamine, could markedly ameliorate steatosis and inflammation, which was mediated by overexpressed TRIM59. Besides, TRIM59 was demonstrated to interact with GPX4 and promoted its ubiquitination. The overexpression of GPX4 could significantly reverse the pathogenic effects of TRIM59 in NAFLD. Additionally, the inhibition of TRIM59 appeared to be a promising strategy to ameliorate NAFLD in mice model. In summary, our study revealed that TRIM59 could promote steatosis and ferroptosis in NAFLD via enhancing GPX4 ubiquitination. TRIM59 could be a potential target for NAFLD treatment.

Bacterial extracellular polymeric substances: Impact on soil microbial community composition and their potential role in heavy metal-contaminated soil.

In this study, six different treatments involving extracellular polymeric substances (EPS) from Enterobacter sp. FM-1 (FM-1) (no EPS (control), original bacterial cells (FM-1), FM-1 cells with EPS artificially removed (EPS-free cells, EPS-R), different forms of EPS (soluble EPS (S-EPS), loosely bound EPS (LB-EPS) and tightly bound EPS (TB-EPS)) obtained from FM-1) and three types of soils (non-contaminated soil (NC soil), high-contamination soil (HC soil) and low-contamination soil (LC soil)) were used to investigate the impact of different EPS treatments on soil microbial community composition and their potential role in the remediation of heavy metal (HM)-contaminated soil. The results indicate that the EPS secreted by FM-1 played a vital role in changing soil pH and helped increase soil bio- HMs. In addition, EPS secretion by FM-1 helped increase the soil EPS-polysaccharide and EPS-nucleic acid contents; even in HC soil, where the HM content was relatively high, LB-EPS addition still increased the EPS-polysaccharide and EPS-nucleic acid contents in the soil by 1.18- and 15.54-fold, respectively. FM-1, LB-EPS and TB-EPS addition increased the soil invertase, urease and alkaline phosphatase activities and increased the soil organic matter (SOM), NH4+-N and available phosphorus (AP) contents, which helped regulate soil nutrient reserves. Moreover, the addition of different EPS fractions modified the soil microbial community composition to help microbes adapt to an HM-contaminated environment. In the HC and LC soils, where the HM content was relatively high, the soil bacteria were dominated by Protobacteria, while fungi in the soil were dominated by Ascomycota. Among the soil physicochemical properties, the soil SOM and NH4+-N contents and invertase activity significantly impacted the diversity and community composition of both bacteria and fungi in the soil.

Effects of Graphene Oxide on Atrazine Phytotoxicity Effects of Graphene Oxide on Photosynthetic Response of Iris Pseudacorus to Atrazine Stress and Accumulation of Atrazine in the Plant.

To evaluate combined effects of co-existed pesticides and nanomaterials on aquatic plants, the toxicity of herbicide atrazine (ATZ) on Iris pseudacorus in the presence and absence of Graphene oxide (GO) was investigated using chlorophyll a fluorescence transients. Results showed that GO reduced ATZ accumulation in plant. ATZ or ATZ combined with GO mainly blocked electron transport beyond QA at PSII as indicated by the sharp rise of the J-step level of fluorescence rise kinetics. The pronounced increase in Fm and the loss of I-step were observed when ATZ was at 2.0 mg·L- 1 implying the damage on the oxygen evolution complex and PSI. GO at environmentally relevant concentration did not exhibit significant photosynthetic inhibitory effects on I. pseudacorus. GO at 1.0 mg·L- 1 promoted photosynthesis of I. pseudacorus under ATZ stress at 2.0 mg·L- 1. These result indicated that the presence of GO alleviated the photosynthesis inhibition by ATZ at high levels.

Phytotoxicity of atrazine combined with cadmium on photosynthetic apparatus of the emergent plant species Iris pseudacorus.

The combined pollution, instead of single pollution, has become a widespread contamination phenomenon in aquatic environment. However, little information is now available about the joint effects of the combined pollution, especially co-existed pesticides and heavy metals, on aquatic plants. In the present study, using continuous excitation chlorophyll fluorescence parameters and the OJIP transient, comparisons of herbicide atrazine (ATZ) phytotoxicity on Iris pseudacorus between in the presence and absence of cadmium (Cd) were evaluated over an exposure period of three weeks under laboratory conditions. Results showed that both ATZ and Cd were toxic to I. pseudacorus. The ratio Fv/Fo, specific electron transport energy (ET0/RC), and photochemistry efficiency (PIabs and PItotal) of this emergent plant species at individual ATZ and Cd concentrations were significantly lower than those of the control. ATZ mainly inhibited electron transport beyond QA at PSII acceptor side as indicated by the sharp rise of the J-step level of fluorescence rise kinetics. A pronounced K-step and the loss of I-step due to the damage on the OEC and PSI also occurred when ATZ was at or above 1.0 mg·L-1. In comparison to ATZ alone, ATZ combined with Cd resulted in a lower amplitude rise in J-step with apparent J-I and I-P phases; and significantly lower Fo with higher Fv/Fo, as well as greater ET0/RC with higher values of PIabs and PItotal. However, the adverse influences of ATZ combined with Cd on the above indicators were still significant as compared with the control. Therefore, the coexistence of Cd alleviated the individual phytotoxicities of ATZ, whereas combined pollution of ATZ and Cd still induced the decline in photosynthetic performance of I. pseudacorus, and its potential ecological impacts on the aquatic vegetation cannot be ignored. Our findings offer a better understanding of the joint effects of the pesticide and heavy metal on non-target aquatic plants, and provided valuable insights into the interaction of these pollutants in aquatic environment.

Variation in Extracellular Polymeric Substances from Enterobacter sp. and Their Pb2+ Adsorption Behaviors.

The objective of this study was to investigate the effects of the cultivation time, temperature, and pH value on the yield and composition of extracellular polymeric substances (EPS) from Enterobacter sp. FM-1 (FM-1) and to analyze the Pb2+ adsorption behavior of soluble EPS (S-EPS), loosely bound EPS (LB-EPS), and tightly bound EPS (TB-EPS). Maximum EPS production was obtained when the cultivation time, temperature, and pH value were 24 h, 30 °C, and 8.0, respectively. The main components of EPS were proteins, polysaccharides, and nucleic acids, but the different EPS types contained different proportions and specific components. The Pb2+ adsorption capacity of LB-EPS was 2.23 and 1.50 times higher than that of S-EPS and TB-EPS, respectively. After Pb2+ adsorption by LB-EPS, the pH value of the reaction system decreased to the lowest of 5.23, which indicated that LB-EPS contained more functional groups that could release H+, which will help to better adsorb Pb2+ through ion exchange. The three-dimensional excitation-emission matrix fluorescence spectroscopy (3D-EEM) analysis showed that the fluorescence intensity of tryptophan-containing substances decreased by 85.5% after Pb2+ adsorption by LB-EPS, which indicated the complexation of tryptophan-containing substances with Pb2+. Fourier transform infrared spectroscopy (FT-IR) and X-ray photoelectron spectroscopy (XPS) O spectra indicated that the C=O peak from protein amide I of tryptophan-containing substances in LB-EPS was mainly responsible for the complexation of Pb2+. After the adsorption of Pb2+, the proportion of the C=O peak in LB-EPS increased by 33.89%, indicating that the complexation of LB-EPS with Pb2+ was mainly attributed to the O atom in the C=O terminus of protein amide I.

Influence of Cd on atrazine degradation and the formation of three primary metabolites in water under the combined pollution.

To understand the influence of Cd on atrazine (ATZ) degradation in aqueous solution, the degradation of different initial levels of ATZ (0.1, 0.5, 1.0, and 2.0 mg·L-1) was investigated in the presence and absence of Cd2+ in a 20-day laboratory experiment. It was found that Cd2+ caused a significant decrease in ATZ degradation and increased its half-life from 17-34 days to 30-57 days (p < 0.0001). Regarding the three most common metabolites of ATZ, deethylatrazine (DEA) and deisopropylatrazine (DIA) were detected in water earlier than hydroxyatrazine (HYA). The DEA content was several times higher than the DIA and HYA contents, regardless of the presence or absence of Cd2+. In the presence of Cd2+, the DIA content was significantly lower and the HYA content was significantly higher. Furthermore, Cd2+ had a dose-dependent effect on HYA formation. Our results indicated that the coexistence of Cd2+ and ATZ resulted in greater herbicide persistence, thereby possibly increasing the risk of environmental contamination. DEA was still the predominant ATZ degradation product detected in water under the combined pollution, which was similar to the ATZ tendency.

ROS/NF-κB Signaling Pathway-Mediated Transcriptional Activation of TRIM37 Promotes HBV-Associated Hepatic Fibrosis.

Hepatic fibrosis is an inflammatory response that leads to liver cirrhosis in the most advanced condition. Liver cirrhosis is a leading cause of deaths associated with liver diseases; hence, understanding the underlying mechanisms of hepatic fibrosis is critical to develop effective therapies. Tripartite motif (TRIM) family proteins have been shown to be involved in liver fibrosis; however, the exact role of several TRIM proteins in this process remained unexplored. In this study, we investigated the role of TRIM37 in hepatitis B virus (HBV)-associated hepatic fibrosis. We analyzed TRIM37 expression in hepatic fibrosis patients and performed functional and mechanistic studies in tissue culture and mouse models to identify the role of TRIM37 in hepatic fibrosis. We found an increased expression of TRIM37 in hepatic fibrosis patients. Mechanistically, we showed that TRIM37 physically interacts with SMAD7 and promotes ubiquitination-mediated degradation of SMAD7, and that SMAD7 is a key mediator of TRM37-induced hepatic fibrosis. Furthermore, we showed nuclear factor κB (NF-κB) activation mediated by reactive oxygen species (ROS) is necessary for the transcriptional induction of TRIM37 during HBV infection. Our study shows TRIM37 as an important promoter of HBV-associated hepatic fibrosis.

Manganese accumulation and plant physiology behavior of Camellia oleifera in response to different levels of potassium fertilization.

The effects of potassium (K) fertilization (KCl, analytically pure; 0, 60, 200, and 400 mg kg-1) on the growth and Mn accumulation of Camellia oleifera in two types of Mn-contaminated soils were investigated. The potential mechanisms underlying the impacts of K fertilization were explored. C. oleifera accumulated high amounts of Mn in both soil conditions. The addition of K fertilizer decreased the soil pH and promoted Mn accumulation in C. oleifera. However, the plant biomass decreased significantly under the high level of K fertilization (400 mg kg-1), and the oxidative stress was stimulated under Mn contamination. But an appropriate concentration of K fertilizer (200 mg kg-1) was necessary for the formation of photosynthesis pigments, nonenzymatic antioxidants and antioxidant enzymes, metabolic processes, and nutrient uptake. Furthermore, when plants supplemented with a low level of K fertilization (200 mg kg-1), the catalase activity in C. oleifera leaves was enhanced to alleviate oxidative stress and protect the plant from Mn contamination. Our study demonstrated that 200 mg kg-1 of K fertilizer has the potential to further enhance the efficiency of Mn phytoremediation by C. oleifera.

Qizhufang (ZSF) Ameliorates Hepatic Iron Overload via Signal Transducer and Activator of Transcription 3 (STAT3) Pathway.

BACKGROUND Iron overload is a prominent characteristic of liver injury, but there is no effective treatment at present. Qizhufang (ZSF) is a Chinese herbal formula showed anti-HBV activities, improved liver function, and anti-fibrosis effect. ZSF showed a series of liver-protection functions, but whether ZSF can relieve hepatic iron overload is still unclear. MATERIAL AND METHODS Ferric ammonium citrate (FAC) was used to construct iron-overloaded LO2 cells. The cell apoptosis and proliferation were measured by flow cytometry and CCK-8 assay, respectively. ROS level was analyzed by fluorescence probe. RNA and protein expressions were assessed by real-time PCR and Western blot. RESULTS FAC upregulated apoptosis rate, ROS level, and expression of hepcidin and p-STAT3, but suppressed proliferation and expression of DMT1, FPN1, and CP in LO2 cells. However, Qizhufang (ZSF) reversed the effect of FAC. We also found that hepcidin overexpression suppressed the expressions of DMT1, FPN1, and CP, which were reversed by ZSF. Additionally, STAT3 inhibitor AG490 suppressed hepcidin expression. Moreover, exogenous IL-6 reversed the effect of ZSF on apoptosis rate, ROS level, and the expression of hepcidin, DMT1, FNP1, CP, and p-STAT3. CONCLUSIONS Qizhufang (ZSF) can ameliorate iron overload-induced injury by suppressing hepcidin via the STAT3 pathway in LO2 cells.

Protective Effect of Astragaloside IV on Hepatic Injury Induced by Iron Overload.

Suitable content of iron is essential for human body, but iron overload is associated with many kinds of diseases including chronic liver damage. Recently, researchers find that iron overload promotes hepatocyte autophagy and apoptosis. However, the mechanism of iron overload in liver damage remains unclear. In this study, Lo2 cells were selected as the research object, iron dextran was a model drug, and astragaloside IV was a therapeutic drug to explore the role of iron overload. MTT assay and Annexin/PI double staining were used to measure cell viability and apoptosis. Ultrastructure was observed by transmission electron microscopy. The expression levels of apoptosis and autophagy-related proteins were determined by real-time PCR and Western Blot. The results showed that iron dextran could significantly inhibit Lo2 cell viability and increase the apoptosis rate, while astragaloside IV could reverse the inhibition of Lo2 cell viability and decrease the apoptosis rate. Transmission electron microscopy showed a significant increase in the number of autophagosomes after administration of iron dextran, and the application of astragaloside IV reduced the production of autophagosomes. LC3II/I was significantly upregulated in the model group but decreased in the astragaloside IV treatment group, and P62 showed the opposite trend. Iron dextran significantly upregulated the expression of Bax and downregulated Bcl2, while astragaloside IV reversed this trend. Finally, the inhibition of hepcidin caused by iron dextran was counteracted by astragaloside IV. In conclusion, the experimental results show that the iron overload model mainly induces excessive autophagy and apoptosis of hepatocytes, thus causing damage to hepatocytes, but astragaloside IV plays a certain therapeutic role in reversing this damage.

ARHGAP10 Inhibits the Proliferation and Metastasis of CRC Cells via Blocking the Activity of RhoA/AKT Signaling Pathway.

INTRODUCTION: ARHGAP10 belongs to the ARHGAP family, which is downregulated in certain human tumors. However, the detailed function of ARHGAP10 remains unclear in human colon carcinoma (CRC). In the current study, we aimed to explore the role of ARHGAP10 in the growth and metastasis of CRC cells. METHODS: ARHGAP10 was induced silencing and overexpression using RNA interference (RNAi) and lentiviral-vector in CRC cells. Quantitative real-time PCR (qRT-PCR) and Western blot were used to quantify the mRNA and protein contents of ARHGAP10. Cell proliferation was determined by using Cell counting kit-8 (CCK-8). Transwell assay was utilized to examine the role of ARHGAP10 in the migration and invasion of CRC cells. RESULTS: Our results indicated that ARHGAP10 was downregulated in human CRC tissues and low expression of ARHGAP10 was associated with poor prognosis of patients with CRC. Moreover, ARHGAP10 overexpression significantly inhibited the proliferation and metastasis of CRC cells. Moreover, a PI3K/AKT inhibitor LY294002 was utilized to examine the connection between ARHGAP10 and AKT. Our findings demonstrated that the AKT inhibitor LY294002 could rescue the function of ARHGAP10 in CRC cells. DISCUSSION: It was the first time to elucidate that AKT involved in the ARHGAP10 signaling pathway and ARHGAP10 negatively mediated the phosphorylation of AKT (p-AKT) and RhoA activity in CRC cells. Interestingly, the Rho/MRTF/SRF inhibitor CCG-1423 significantly inhibited the phosphorylation of AKT in ARHGAP10 siRNA transfected CRC cells. Much importantly, overexpression of ARHGAP10 deeply suppressed the metastasis of CRC cells in the lung in vivo. Taken together, our findings not only enhanced the understanding of the anti-cancer effect of ARHGAP10 in CRC cells but also indicated its underlying pathway in CRC.