Dibutyl phthalate (DBP) is one of the most widely used phthalate esters (PAEs) that raise increasing ecotoxicological concerns due to their harmful effects on living organisms and ecosystems. Recently, while PAEs pollution in the Yangtze River has attracted significant attention, little research has been conducted on the impact of PAEs stress on S. prenanti, an endemic and valuable species in the Yangtze River. In this study, one control group (C-L) and three experimental groups: T1-L (3 mu g/L), T2-L (30 mu g/L), and T3-L (300 mu g/L) were established with reference to the DBP concentration in the environment. For the first time, we investigated the effects of DBP stress on the liver of S. prenanti using histomorphological, physiological, and biochemical indexes, as well as a joint multi-omics analysis. The results revealed that compared to the C-L group, liver structural damage and stress were not significant in the environmental concentration group (T1-L) and the number of differential genes and differential metabolites were lower. However, as DBP stress concentration increased, the liver damage became severe, with significant vacuolation and hemolysis observed in the T2-L and T3-L groups. The TUNEL assay revealed a significant increase in the number of apoptotic cells along with a notable rise in differential genes and metabolites in the T2-L and T3-L groups. Oxidative stress markers (T-AOC, SOD, CAT, and GSH-PX) were also significantly higher in the T2-L and T3-L groups. RNA-Seq analysis showed that the protein processing in the endoplasmic reticulum pathway was most significantly-enriched differential gene pathway shared by both C-L vs T2-L and C-L vs T3-L, with most of the genes in this pathway showing significant up-regulation. This suggests that the protein processing in the endoplasmic reticulum pathway may play a key role in protecting the liver from injuries caused by high DBP stress. Interestingly, C XI, C XII, C XIII, C XIV and C XV in the chemical carcinogenesis-reactive oxygen species pathway were significantly down-regulated in the T2-L and T3-L groups based on combined transcriptomic and metabolomic analyses, suggesting that DBP causes liver injury by disrupting mitochondria. This comprehensive histomorphometric and multi-omics study demonstrated that the current DBP concentration in the habitat of S. prenanti in the upper reaches of the Yangtze River temporarily causes less liver damage. However, with increasing of DBP concentration, DBP could still cause serious liver damage to S. prenanti. This study provides a new mechanistic understanding of the liver response mechanism of S. prenanti under different concentrations of DBP stress and offers basic data for the ecological protection of the Yangtze River.

Wireworms are the most destructive soil insect pests affecting horticultural crops. The damage often renders them unsuitable for commercial purposes, resulting in substantial economic losses. RNA interference (RNAi) has been broadly used to inhibit gene functions to control insect populations. It employs double-stranded RNA (dsRNA) to knockdown essential genes in target organisms, rendering them incapable of development or survival. Although it is a robust approach, the primary challenges are identifying effective target genes and delivering their dsRNA into wireworms. Thus, the present study established a liquid ingestion methodology that efficiently delivers dsRNA into wireworms. We then investigated the effects of four target genes on wireworm mortality. The highest mortality rate reached 50% when the gene encoding vacuolar ATPase subunit A was targeted. Its transcript content in the fed wireworms was also significantly reduced. The mortality rates of the other three target genes of vacuolar ATPase subunit E, beta-actin, and chitin synthase 1 were 28%, 33%, and 35%, respectively. This is the first report demonstrating an efficient feeding methodology and the silencing of target genes in wireworms. Our findings indicate that RNAi is an effective alternative method for controlling the wireworm pest, and can be used to develop field treatment strategies.

Background: Heavy elements such as antimony greatly affect the environment and living organisms. Antimony is discharged into the environment by mining and industries that use it as pesticides and flame retardants. This activity can lead to environmental pollution, water and soil contamination. Antimony can also accumulate in living organisms and cause negative health effects, such as damage to the respiratory system and skin, and growth abnormalities of animals and plants. Methods : The primary objective of this investigation was to explore the teratogenic impact of the antimony heavy metal on histological structure of the liver in adult rabbits ( Oryctolagus cuniculus ). The study included adult white rabbits divided into several groups: the first one is the control group injected with physiological saline (0.09% NaCl), the other group injected with 20 mg/kg antimony, and the last injected with 30 mg/kg antimony over a 30 -day period. Following this, postmortem procedures were conducted to extract and fix the liver organ, and tissue sections were prepared. Result : The results revealed significant histological changes, including distortion and rupture in Glisson's Capsule, leading to the formation of a sub -capsular space due to its separation from hepatocytes. Additionally, alterations in the radial organization of hepatocytes and pyknosis in the nuclei were observed, characterized by a dark color and reduced size. Karyolysis, where nuclei completely disappeared, and hydropic degeneration in hepatocytes with swollen appearance and dark nuclei due to fluid accumulation were noted. Moreover, an increase in Kupffer cells and blood congestion in the central vein, resulting in dilation compared to the control group, were observed. Conclusion : Overall, the treatment with antimony at 20 and 30 mg/g doses for 30 days show profound teratogenic effects on the histological structure of the liver in adult rabbits. These effects are represented by the destruction of various parts of liver, in addition to changes in arrangement, and distortion and rupture of the cells. Furthermore, an increase in Kupffer cells and blood congestion were also recorded.

Although selenium (Se) and cadmium (Cd) often coexist naturally in the soil of China, the health risks to local residents consuming Se-Cd co -enriched foods are unknown. In the present study, we investigated the effects of chemical -based selenocystine (SeCys2) on cadmium chloride -induced human hepatocarcinoma (HepG2) cell injury and plant (Cardamine hupingshanensis)-derived SeCys2 against Cd-induced liver injury in mice. We found that chemical- and plant -based SeCys2 showed protective effects against Cd-induced HepG2 cell injury and liver damage in mice, respectively. Compared with Cd intervention group, co -treatment with chemical- or plant -based SeCys2 both alleviated liver toxicity and ferroptosis by decreasing ferrous iron, acyl-CoA synthetase long -chain (ACSL) family member 4, lysophosphatidylcholine acyltransferase 3, reactive oxygen species and lipid peroxide levels, and increasing ACSL3, peroxisome proliferator-activated receptor alpha, solute carrier family 7 member 11 (SLC7A11) and glutathione and glutathione peroxidase 4 (GPX4) levels. In conclusion, chemical- and plant -based SeCys2 alleviated Cd-induced hepatotoxicity and ferroptosis by regulating SLC7A11/GPX4 signaling and lipid peroxidation. Our findings indicate that potential Cd toxicity from consuming foods grown in Se- and Cd-rich soils should be re-evaluated. This study offers a new perspective for the development of SeCys2-enriched agricultural products.

Animal experiments suggest that selenium (Se) may alleviate cadmium (Cd) toxicity in animal liver and kidneys, but its effect on human liver and kidneys remains uncertain. In China, areas with black shale have shown elevated levels of Se and Cd. According to the USEPA (U.S. Environmental Protection Agency) evaluation method, the soil and rice in these areas pose significant risks. In black shale regions such as Enshi and Zhuxi County, residents who long-term consume local rice may surpass safe Se and Cd intake levels. Significantly high median blood Se (B-Se) and urine selenium (U-Se) levels were detected in these areas, measuring 416.977 mu g/L and 352.690 mu g/L and 104.527 mu g/L and 51.820 mu g/L, respectively. Additionally, the median blood Cd (B-Cd) and urine Cd (U-Cd) levels were markedly elevated at 4.821 mu g/L and 3.848 mu g/L and at 7.750 mu g/L and 7.050 mu g/L, respectively, indicating substantial Cd exposure. Nevertheless, sensitive liver and kidney biomarkers in these groups fall within healthy reference ranges, suggesting a potential antagonistic effect of Se on Cd in the human body. Therefore, the USEPA method may not accurately assess Cd risk in exposed black shale areas. However, within the healthy ranges, residents in the Enshi study area had significantly greater median levels of serum creatinine and cystatin C, measuring 67.3 mu mol/L and 0.92 mg/L, respectively, than those in Zhuxi did (53.6 mu mol/L and 0.86 mg/L). In cases of excessive Se and Cd exposure, high Se and Cd levels impact the filtration function of the human kidney to some extent. Se is an essential trace element for humans. However, excessive intake of Se can harm humans. Cd is a carcinogen and a chronic potent nephrotoxin that mostly accumulates in the human liver and kidneys. Animal experiments suggest that Se may alleviate Cd toxicity in animal liver and kidneys, but its effect on human liver and kidneys remains uncertain. In China, areas with black shale exposure have shown elevated levels of Se and Cd. According to the USEPA (U.S. Environmental Protection Agency) evaluation method, the soil and rice in these areas pose significant risks. Our results suggested that the exposed black shale areas are simultaneously enriched with Se and Cd. However, residents in these areas were exposed to excessive Se and Cd long-term without significant damage to liver and kidney functions. Therefore, the USEPA method may not accurately assess Cd risk in exposed black shale areas. The risk assessment of heavy metals in high-Se geological background areas cannot be separated from human health surveys. Our study provides evidence for the antagonistic effects of Se and Cd on the human body. Residents in exposed black shale areas consume excessive Se and Cd through local rice Human liver and kidney functions are not significantly damaged in exposed black shale areas The USEPA method may not accurately assess Cd risk in exposed black shale areas

As typical antibiotics, tetracycline (TC) and sulfadiazine (SDZ) enter the human body through the food chain. Therefore, it is necessary to understand their individual and combined toxicity. In this study, the effects of TC, SDZ, and their mixture on cell viability, cell membrane damage, liver cell damage, and oxidative damage were evaluated in in vitro assays with human liver cells Huh-7. The results showed cytotoxicity of TC, SDZ, and their mixture, which induced oxidative stress and caused membrane and cell damage. The effect of antibiotics on Huh7 cells increased with increasing concentration, except for lactate dehydrogenase (LDH) activity that commonly showed a threshold concentration response and cell viability, which commonly showed a biphasic trend, suggesting the possibility of hormetic responses where proper doses are included. The toxicity of TC was commonly higher than that of SDZ when applied at the same concentration. These findings shed light on the individual and joint effects of these major antibiotics on liver cells, providing a scientific basis for the evaluation of antibiotic toxicity and associated risks.

Soil and water pollution are current global environmental and agricultural challenges, adversely affected by ineffective industrial waste treatment before discharging into the environment combined with inefficient long-term inputs of fertilizers. The development of targeted fertilizers delivery vehicles, sufficient soil/water remediation, and contamination detection systems using eco-friendly technologies become critically important. Due to their high specific surface area, biocompatibility, easiness of operation, and high performance, nanomaterials-based controllable soil fertility promoters, adsorbents, sensors, and photocatalysts are promising tools for soil/water pollution prevention, remediation, and monitoring. Altogether, crystallinity, hydrophilic-tunable surface chemistry, and 3D forming ability of nanocellulose (NC), in addition to biodegradability, regeneration ability, and mechanical properties of NC nanocomposite hydrogels (NCHs), lead to advancing promising soil/water nanohydrogels-based targeted fertilizers delivery vehicles, adsorbents, co-adsorbents/co-sensors, and co-adsorbents/co-photocatalysts. In these systems, NCHs introduce 3D rigid porous scaffolds for homogenous dispersing/fixing of functional groups, fertilizers, fluorescence sources, and photocatalysts. Also, they present stimuli-responsive networks for fertilizer regulation in soil, and matrixes with extra active sites enabling contaminates immobilization/degradation. This review outlines an update of the most recent potential utilization of functionalized NCHs-based soil/water adsorbents, photocatalysts, sensors, and slow/targeted fertilizers release vehicles. An in-depth discussion of surface pretreatments-modifications used to improve their performance, fabrication methods, application properties, and working mechanisms was discussed. The potential limitations and future perspectives on using NCHs in fertilizer/water management, soil/water remediation, and detection are highlighted.

Background: Gut microbiome dysbiosis is related to the pathogenesis of nonalcoholic fatty liver disease (NAFLD), and the role of toll-like receptor 2 (TLR2) in its molecular mechanism is controversial. Here, we investigated the effects and mechanisms of Escherichia coli-derived lipopolysaccharide (LPS) on lipid accumulation and lipotoxicity in palmitic acid (PA)-treated L02 cell as an NAFLD cell model, and the role of TLR2 in this process. Methods: Oil red O staining assay and free fatty acid (FFA) content test were performed to determine the effects of LPS on lipid accumulation in a PA-induced NAFLD cell model with or without TLR2 inhibition. The levels of IL-6 and TNF-alpha were measured to investigate inflammation conditions. Hoechst 33342 staining assay and Caspase-3 activity assay were used to test cell apoptosis, and the expression levels of proteins in the IRS1/PI3K/AKT signaling pathway, TLR2/MyD88/IKK alpha/NF-kappa B signaling pathway, and mitochondrion-dependent apoptotic signaling pathway were detected using Western blot. Results: Lipid accumulation, pro-inflammatory cytokine release, and cell apoptosis with high levels were observed in the PA-induced NAFLD cell model, and LPS aggravated these processes. Whereas TLR2 inhibition could significantly ameliorate PA-induced and LPS-amplified lipid accumulation, inflammatory, and cell apoptosis, it had no significant effect on L02 cells treated with LPS alone. Conclusions: These results were confirmed by activation or inhibition of the IRS1/PI3K/AKT signaling pathway, TLR2/MyD88/IKK alpha/NF-kappa B signaling pathway, and mitochondrion-dependent apoptotic signaling pathway, and were reflected by changes on their proteins expression. TLR2 is involved in PA-induced lipid accumulation and lipotoxicity in L02 cells, which could be aggravated by LPS, although LPS-induced amplification might not be through direct interaction with TLR2.