Identification of water pollution sources and analysis of pollution trigger conditions in Jiuqu River, Luxian County, China.

Against the backdrop of ecological conservation and high-quality development in the Yangtze River Basin, there is an increasing demand for enhanced water pollution prevention and control in small watersheds. To delve deeper into the intricate relationship between pollutants and environmental features, as well as explore the key factors triggering pollution and their corresponding warning thresholds, this study was conducted along the Jiuqu River, a strategically managed unit in the upstream region of the Yangtze River, between 2022 and 2023. A total of seven monitoring sites were established, from which 161 valid water samples were collected. The k-nearest neighbors mutual information (KNN-MI) technique indicated that water temperature (WT) and relative humidity (RH) were the main environmental factors. The principal component analysis (PCA) of ten water quality parameters and three environmental factors unveiled the distinguishing characteristics of the primary pollution sources. Consequently, the pollution sources were categorized as treated wastewater > groundwater runoff > phytoplankton growth > abstersion wastewater > agricultural drainage. Furthermore, the regression decision tree (RDT) algorithm was used to explore the combined effects between pollutants and environmental factors, and to provide visual decision-making process and quantitative results for understanding the triggering mechanism of organic pollution in Jiuqu River. It conclusively identifies total phosphorus (TP) as the predominant triggering parameter with the threshold of 0.138 mg/L. The study is helpful to deal with potential water pollution problems preventatively and shows the interpretability and predictive performance of the RDT algorithm in water pollution prevention.

[Sodium nitrite reduces lipid accumulation in steatotic cells by enhancing autophagy].

Recent data have revealed that inhibiting autophagy exacerbates lipid accumulation in hepatocytes and nitrite treatment reduces total triglyceride levels in the high-fat diet mice. Therefore, the present study aimed to determine the effects of nitrite on simple hepatic steatosis and the possible role of autophagy. Firstly, steatotic L-02 cells were induced by incubating L-02 cells with 1.2 mmol · L(-1) oleic acid (OA) for 24 h. Secondly, steatotic L-02 cells were treated with 0.2 mmol · L(-1) sodium nitrite (SN) plus 3-methyladenine (3-MA), or chloroquine (CQ) for 24 h, and then lipid accumulation was measured with oil red O staining and triglyceride quantification. The notable steatosis could be observed in L-02 cells following exposure to 1.2 mmol · L(-1) OA for 24 h. Treatment with 0.2 mmol · L(-1) sodium nitrite reduced lipid accumulation in steatotic L-02 cells. 3-MA weakened the ability of sodium nitrite to ameliorate hepatic steatosis. Additionally, the sodium nitrite increased number of LC3-II immunostaining puncta and LC3-II protein expression was confirmed by immunofluorescence or Western blot analysis, and the effects were enhanced by CQ treatment. The number of increased cytoplasm vacuoles and lysosomes increased was confirmed by phase contrast and fluorescence microscope respectively. The increased autolysosome was detected by electron microscopy, this phenomenon could be reversed by CQ treatment. These data demonstrated that sodium nitrite enhanced the autophagic flux and decomposition of triglycerides in steatotic L-02 cells.

Exogenous hydrogen sulfide mitigates the fatty liver in obese mice through improving lipid metabolism and antioxidant potential.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. Hydrogen sulfide (H2S) plays an important role in physiology and pathophysiology of liver. However, whether exogenous H2S could mitigate the hepatic steatosis in mice remains unclear. The aim of this study is to evaluate the effects of H2S on fatty liver. METHODS: C57BL/6 mice were fed with either a high-fat diet (HFD) or a normal fat diet (NFD) for 16 weeks. After 12 weeks of feeding, the HFD-fed mice were injected one time per day with NaHS or saline for the followed 4 weeks. RESULTS: Compared to NFD, HFD could induce an accumulation of lipids in liver and a damage of hepatic structure. Compared to saline treatment, in the liver of HFD fed mice H2S treatment could significantly (1) recover the structure; (2) decrease the accumulation of lipids including triglyceride (TG) and total cholesterol (TC); (3) decrease the expression of fatty acid synthase (FAS) and increase the expression of carnitine palmitoyltransferase-1 (CPT-1); (4) reduce malondialdehyde (MDA) levels; (5) increase the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx). CONCLUSION: H2S could mitigate the fatty liver by improving lipid metabolism and antioxidant potential in HFD-induced obese mice.