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.

Apart from directly affecting the growth and development of crops, Cd in the soil can easily enter the human body through the food chain and pose a threat to human health. Therefore, understanding the toxicity of Cd to specific crops and the molecular mechanisms of their response to Cd is essential. In this study, hydroponic experiments were utilized to study the response of foxtail millet to Cd stress through phenotypic investigation, enzyme activity determination, ultrastructure, ionome, transcriptome and metabolome. With the increase in cadmium concentration, both the growth and photosynthetic capacity of foxtail millet seedlings are severely inhibited. The ultrastructure of cells is damaged, cells are deformed, chloroplasts swell and disappear, and cell walls thicken. Cd stress affects the absorption, transport, and redistribution of beneficial metal ions in the seedlings. Multi-omics analysis reveals the crucial roles of glycolysis, glutathione metabolism and phenylpropanoid and lignin biosynthesis pathways in Cd detoxification via energy metabolism, the antioxidant system and cell wall changes. Finally, a schematic diagram of foxtail millet in response to Cd stress was we preliminarily drew. This work provides a basic framework for further revealing the molecular mechanism of Cd tolerance in foxtail millet.

Juglans sigillata, an endemic species in China, serves as a vital local economic resource. Aluminum (Al) stress caused by soil acidification can potentially threaten the growth of J. sigillata. This study aimed to elucidate the mechanism of the alleviation of Al stress by silicon (Si) in J. sigillata. The results showed that Si could reduce the Al accumulation of walnut and improve root growth under Al stress. Si also increased peroxidase (POD), superoxide dismutase (SOD), and catalase (CAT) activities and soluble sugar and proline contents, reduced malonaldehyde (MDA) and H2O2 contents and the O2- production rate, and maintained the homeostasis of cells. Transcriptome analysis revealed significant up-regulation of genes encoding plant hormones (ABA, IAA, and CTK) and photosystem II components (PsbO, PsbQ, PsbW, and PsbY). Under Al stress conditions, the application of exogenous Si notably enhanced the expression of genes associated with heavy metal transport (CAX, PAA, ABC, HMA, NRAMP, and ZIP). Comprehensive transcriptome and metabolomics analysis showed that Si regulated secondary metabolite metabolism via the phenylalanine, galactose, and tryptophan pathway, altered cell wall composition, increased energy supply, and reduced auxin synthesis in root tip transition zones to alleviate Al toxicity of J. sigillata. In summary, the application of Si significantly alleviated Al-induced damage in J. sigillata.

BackgroundSalt stress is considered to be one of the major abiotic stresses influencing rice growth and productivity. To improve rice crop productivity in saline soils, it is essential to choose a suitable variety for mitigating salt stress and gain a deep understanding of the underlying mechanisms. The current study explored the salt tolerance mechanism of wild rice 'HD96-1 (salt resistive)' and conventional rice 'IR29 (salt sensitive)' by evaluating morph-physiological, transcriptomic, and metabolomic approaches.ResultsPhysiological data indicated that HD96-1 had higher chlorophyll content, higher photosynthetic efficiency, more stable Na+/K+, less H2O2, and lower electrolyte leakage under salt stress compared with IR29. Transcriptomic and metabolomic data showed that the expression of NHXs in IR29 was significantly down-regulated under salt stress, leading to a large accumulation of Na+ in the cytoplasm, and that the expression of CHLH, PORA, and PORB was significantly down-regulated, inhibiting chlorophyll synthesis. HD96-1 maintained the balance of Na+ and K+ by increasing the expression of NHX4, and there was no significant change in the expression of genes related to chlorophyll synthesis, which made HD96-1 more resistant to salt stress than IR29. In addition, HD96-1 inhibited the excessive synthesis of hydrogen peroxide (H2O2) and alleviated oxidative damage by significantly down-regulating the expression of ACX4 under salt stress. HD96-1 promoted the accumulation of isoleucine by up-regulating genes of branched-chain amino acid aminotransferase 2 and branched-chain amino acid aminotransferase 4 and might promote the synthesis of raffinose and stachyose by up-regulating the expression of the gene for galactitol synthase 2, which, in turn, maintained a stable osmotic pressure and relieved osmotic stress. We also found that IR29 and HD96-1 alleviated the inhibition of photosynthesis by salt stress by down-regulating the expression of light-harvesting chromophore protein complex (LHCH II)-related genes and reducing the excessive accumulation of glucose metabolites, respectively. In addition, HD96-1 enhances salt tolerance by regulating C2H2 and bHLH153 transcription factors.ConclusionUnder salt stress, HD96-1 maintained ionic balance and photosynthetic efficiency by up-regulating the expression of NHX4 gene and reducing the overaccumulation of glucose metabolites, respectively, and mitigated osmotic stress and oxidative stress by down-regulating the expression of ACX4 and promoting the accumulation of isoleucine, respectively, thereby enhancing the adaptability to salt stress. IR29 maintained photosynthetic efficiency under salt stress by down-regulating the expression of light-harvesting chromophore protein complex (LHCH II)-related genes, thereby enhancing adaptation to salt stress.

Both copper (Cu) excess and boron (B) deficiency are often observed in some citrus orchard soils. The molecular mechanisms by which B alleviates excessive Cu in citrus are poorly understood. Seedlings of sweet orange (Citrus sinensis (L.) Osbeck cv. Xuegan) were treated with 0.5 (Cu0.5) or 350 (Cu350 or Cu excess) mu M CuCl2 and 2.5 (B2.5) or 25 (B25) mu M HBO3 for 24 wk. Thereafter, this study examined the effects of Cu and B treatments on gene expression levels revealed by RNA-Seq, metabolite profiles revealed by a widely targeted metabolome, and related physiological parameters in leaves. Cu350 upregulated 564 genes and 170 metabolites, and downregulated 598 genes and 58 metabolites in leaves of 2.5 mu M B-treated seedlings (LB2.5), but it only upregulated 281 genes and 100 metabolites, and downregulated 136 genes and 40 metabolites in leaves of 25 mu M B-treated seedlings (LB25). Cu350 decreased the concentrations of sucrose and total soluble sugars and increased the concentrations of starch, glucose, fructose and total nonstructural carbohydrates in LB2.5, but it only increased the glucose concentration in LB25. Further analysis demonstrated that B addition reduced the oxidative damage and alterations in primary and secondary metabolisms caused by Cu350, and alleviated the impairment of Cu350 to photosynthesis and cell wall metabolism, thus improving leaf growth. LB2.5 exhibited some adaptive responses to Cu350 to meet the increasing need for the dissipation of excessive excitation energy (EEE) and the detoxification of reactive oxygen species (reactive aldehydes) and Cu. Cu350 increased photorespiration, xanthophyll cycle-dependent thermal dissipation, nonstructural carbohydrate accumulation, and secondary metabolite biosynthesis and abundances; and upregulated tryptophan metabolism and related metabolite abundances, some antioxidant-related gene expression, and some antioxidant abundances. Additionally, this study identified some metabolic pathways, metabolites and genes that might lead to Cu tolerance in leaves.

In acidic soils, aluminum (Al) toxicity inhibits the growth and development of plant roots and affects nutrient and water absorption, leading to reduced yield and quality. Therefore, it is crucial to investigate and identify candidate genes for Al tolerance and elucidate their physiological and molecular mechanisms under Al stress. In this study, we identified a new gene OsAlR3 regulating Al tolerance, and analyzed its mechanism from physiological, transcriptional and metabolic levels. Compared with the WT, malondialdehyde (MDA) and hydrogen peroxide (H2O2) content were significantly increased, superoxide dismutase (SOD) activity and citric acid (CA) content were significantly decreased in the osalr3 mutant lines when exposed to Al stress. Under Al stress, the osalr3 exhibited decreased expression of antioxidant-related genes and lower organic acid content compared with WT. Integrated transcriptome and metabolome analysis showed the phenylpropanoid biosynthetic pathway plays an important role in OsAlR3-mediated Al tolerance. Exogenous CA and oxalic acid (OA) could increase total root length and enhance the antioxidant capacity in the mutant lines under Al stress. Conclusively, we found a new gene OsAlR3 that positively regulates Al tolerance by promoting the chelation of Al ions through the secretion of organic acids, and increasing the expression of antioxidant genes.

Copper is an environmental pollutant, and copper in aquatic environments mainly comes from soil and water. It enters the environment through atmospheric deposition, sewage discharge, and industrial production, and enters aquatic organisms, causing toxicity. Takifugu rubripes (T. rubripes) is a marine fish with high economic value. Due to the toxic effects of heavy metals on aquatic organisms such as fish, it can affect the gut community and metabolites of fish. The gut is an important channel for fish to communicate with the outside world and a necessary pathway for the metabolism of nutrients and toxic substances in the fish body. Studies have shown that due to changes in global water emissions and the high sensitivity of aquatic organisms to the environment, copper may pose greater potential hazards to aquatic organisms. Copper poses a greater risk to aquatic species than other heavy metals and metal/metal like pollutants (such as cadmium, lead, mercury, arsenic, etc.) . In order to elucidate the effects of copper exposure on the gut of T. rubripes. In this study, we exposed T. rubripes to 0, 50, 100, or 500 mu g/L of copper for three days, the effects of copper exposure on the gut microbiota structure and metabolites of the T. rubripes were investigated using 16 S rRNA gene and metabolomics techniques. The research results indicate that with the increase copper concentration, the intestinal tissue of T. rubripes undergoes significant damage. 16 S rRNA sequencing results show that copper exposure alters the structure and metabolites of intestinal microbiota. Copper exposure of 100 and 500 mu g/L inhibited the colonization of the bacterial gut, disrupted the intestinal barrier, and made the fish susceptible to the pathogens. Liquid chromatography-mass spectrometry analysis showed that copper regulated the production of metabolites such as L-histidine, arachidonic acid, and L-glutamic acid, which are related to energy and immunity. Microbiome-metabolome correlation analysis showed that Subdoligranulum, Family_XIII_AD3011_group, and Clostridium_sensu_stricto_1 were the key bacteria for copper ion intervention, and they might up-regulate the levels of metabolites such as indole-3acetic acid, 3-indoleacrylic acid, and 5-hydroxyindole in the tryptophan metabolism pathway. In summary, our research has demonstrated that copper exposure can cause pathological changes in the intestinal tissue of the T. rubripes. High concentrations of copper ions can affect the colonization of the T. rubripes microbiota in the intestine, damage the fish's immune system, and alter the structure and metabolites of the intestinal microbiota, this can lead to intestinal metabolic dysfunction. providing a reference for the evaluation of the biological toxicity effects of heavy metal elements in the marine environment. This study provides a reference for evaluating the biological toxicity effects of heavy metal elements in marine environments.

The effects of co-exposure to aged submicron particles (aSMPs) and Cd as model contaminants on rice leaves via the foliar route were investigated. Thirty-day-old rice seedlings grown in soil were exposed to Cd (nitrate) through foliar spraying at concentrations of 1, 10, 50, 100, and 500 mu M, with or without aSMP at a rate of 30 mu g d-1. It was observed that Cd translocated from leaves to roots via stems even without co-exposure to SMP. Co-exposure can reduce cadmium levels in leaves. Laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS) analysis confirmed a significant reduction (29.3 -77.9%) in Cadmium accumulation in the leaves of rice plants during co-exposure. Exposure to Cd resulted in physiological, transcriptomic, and metabolomic changes in rice leaves, disrupting 28 metabolism pathways, and impacting crop yield and quality. Exposure to both Cd and aSMPs can interfere with the Cd distribution in plants. Rice leaves exposed solely to Cd exhibit higher toxicity and Cd accumulation, compared to those co-exposed to Cd and aSMPs. The accumulation of Cd in plant leaves is enhanced with aSMPs, which may lead to more pronounced gene expression regulation and changes in metabolic pathways, compared to Cd exposure. Our study found that the independent Cd exposure group had higher Cd accumulation and toxicity in rice leaves compared to the combined exposure of Cd and aSMPs. We hypothesize that aged negatively charged SMPs can capture Cd and reduce its exposure in the free state while jointly inhibiting Cd-induced oxidative and chloroplast damage, thereby reducing the potential risk of Cd exposure in rice plants.

Both microplastics (MPs) and cadmium (Cd) are common contaminants in farmland systems, is crucial for assessing their risks for human health and environment, and little research has focused on stress responses mechanisms of crops exposed to the combined pollution. The present study investigated the impact of poly-ethylene (PE) and polypropylene (PP) microplastics (MPs), in combination with Cd, on the physiological and metabolomic changes as well as rhizosphere soil of potherb mustard. Elevated levels of PEMPs and PPMPs were found to impede nutrient uptake in plants while promoting premature flowering, and the concomitant effect is lower crop yields. The substantial improvement in Cd bioavailability facilitated by MPs in rhizosphere soil, especially in high concentrations of MPs, then elevated bioavailability of Cd contributed to promoted Cd accumulation in plants, with distinct effects depending on the type and concentration of MPs. The presence of MPs Combined exposure to high concentrations of MPs and Cd resulted in alterations in plant physiology and metabolomics, including decreased biomass and photosynthetic parameters, elevated levels of reactive oxygen species primarily H2O2, increased antioxidant enzyme activities, and modifications in metabolite profiles. Overall, our study assessed the potential impact on food security (the availability of cadmium to plant) and crops stress responses regarding the contamination of MPs and Cd, providing new insights for future risk assessment in agriculture.