Lead (Pb) and copper (Cu) frequently co-occur in aquatic environments, yet their combined neurotoxic mechanisms remain unclear. Here, zebrafish (Danio rerio) larvae were exposed to environmentally relevant concentrations of Pb (10 μg/L) and Cu (20 μg/L) to assess neurobehavioral and molecular effects. Co-exposure reduced locomotor activity, altered stress-related behavioral responses, and increased developmental abnormalities. Acetylcholinesterase activity was suppressed, accompanied by elevated lipid peroxidation and disrupted antioxidant defenses. Apoptosis was activated via Bax/Bcl-2/Caspase-3 modulation, with downregulation of neurodevelopmental and neurotransmission marker genes. Ferroptosis emerged as a significant contributor to Pb + Cu neurotoxicity, as indicated by dysregulation of nrf2, keap1, and gpx4. Mitochondrial dysfunction was evident through reduced ATP, impaired biogenesis, disrupted electron transport, and excessive fission. Inflammation was mediated via NF-κB/p38-MAPK pathway, with upregulation of pro-inflammatory cytokines and altered anti-inflammatory markers. Western blotting confirmed activation of Nrf2/Keap1/HO-1 signaling axis, highlighting the functional role of ferroptosis in Pb- and Cu-induced neurotoxicity. Importantly, treatment with the ferroptosis inhibitor ferrostatin-1 partially alleviated oxidative damage and neurobehavioral deficits, supporting a contributory role of ferroptosis in the observed effects. Overall, these findings indicate that co-exposure to Pb and Cu induces neurotoxicity in zebrafish larvae through interconnected pathways involving oxidative stress, mitochondrial dysfunction, and ferroptosis-associated processes. This study highlights the ecological relevance of metal co-exposure and its potential risks to aquatic organisms.

Smaller polystyrene nanoplastics (PS-NPs) can act as vectors for co-existing environmental heavy metals like lead (Pb). The complex neurological health risks posed by these co-exposures are concerning, but their combined neurotoxicity mechanism remains unclear. This study investigated the individual and combined toxic impacts of PS-NPs (5 mg/kg in mice, 50 μg/mL in HT22 cells) and Pb (100 mg/L in mice, 10 μg/mL in HT22 cells) on hippocampal neurons, and explored the underlying mechanisms. The results show that PS-NPs facilitate Pb accumulation in the mouse hippocampus and HT22 cells via clathrin-mediated endocytosis. Co-exposure to Pb and PS-NPs, but not either alone, synergistically induced hippocampal neuronal damage, manifesting as synaptic loss and memory deficits in mice, and triggered S-phase cell cycle arrest alongside oxidative stress in HT22 cells. Mechanistically, Pb+PS-NPs caused mitochondrial dysfunction and shifted mitochondrial dynamics towards excessive fission, evidenced by upregulated DRP1/p-DRP1Ser616 and downregulated MFN1/2, and activated PINK1/Parkin-mediated mitophagy. Crucially, inhibition of this mitochondrial fission-mitophagy axis by Mitochondrial Division Inhibitor 1 or cyclosporin A attenuated mitochondrial damage, rescued S-phase arrest, and alleviated hippocampal neuronal injury. Our findings unveil a novel pathway wherein the mitochondrial fission-mitophagy axis drives neuronal cell cycle arrest and cognitive impairment, providing new insights into the risks of combined pollutant exposure.

Although acetamiprid causes testicular toxicity in non-target animals, its low-dose toxicity mechanisms remain poorly understood, leading to underestimated ecological risks. This study demonstrates that low-dose acetamiprid exposure causes testicular toxicity by disrupting lipophagic homeostasis. Even at 0.07 mg/kg, acetamiprid induced significant testicular impairment, characterized by seminiferous epithelial disruption and excessive lipid droplet (LD) accumulation. Cellular analyses identified Sertoli cells as the primary targets, leading to severe lipotoxicity. Mechanistically, acetamiprid activated the PI3K/AKT/mTOR signaling pathway, thereby impairing lipophagic flux. The impairment was induced by increased LD diameter and p62 accumulation, which hindered LD degradation. Furthermore, the upstream initiator TLR4 facilitated extracellular signal transduction to mTOR. By elucidating these mechanisms, this study highlights the reproductive risks of acetamiprid to non-target mammals, supporting ecological risk assessment and environmental management in agricultural ecosystems.

High temperature (HT) poses a significant threat to aquatic organisms, yet the molecular mechanisms underlying HT-induced reproductive impairment in fish remain unclear. In this study, we demonstrated that both short-term (< 21 days) and long-term (> 120 days) exposure to HT (33℃) induced reproductive dysfunction in male zebrafish, including reduced fertilization rates, impaired sperm quality, inhibited testicular development, and increased offspring mortality. Transcriptome analyses showed that short-term HT exposure primarily disrupted testicular energy metabolism, whereas long-term exposure impaired sperm-egg recognition and binding. By analyzing differentially expressed genes involve in reproductive processes, we detected a significant downregulation of testis-specific serine kinase 6 (tssk6) in zebrafish testis under HT conditions. Notably, injection of tssk6-mRNA partially restored the HT-induced reduction in sperm quality. Further investigation revealed that long-term HT increased DNA methylation in the tssk6 promoter region, thereby inhibiting its expression, suggesting tssk6 as a potential biomarker for reproductive health. These findings establish an epigenetic mechanistic link between environmental HT and reproductive function in aquatic organisms.

Background: Brominated flame retardants (BFRs) and per-fluoroalkyl substances (PFAS), are globally concerned persistent toxic substances (PTS) with high co-exposure risks due to their coexistence in the environment matrices and even in humans. However, their combined toxicity hasn't been explored yet. The respective representatives tetrabromobisphenol A (TBBPA) and perfluorooctanoic acid (PFOA) share similar exposure routes and properties of substantial bioaccumulation and environmental persistence. Objectives: To investigate the combined toxicity of BFRs and PFAS with TBBPA and PFOA as the research subjects, and elucidate the mechanisms responsible for the combined toxicity. Methods: Combined toxicity were evaluated after co-exposure with TBBPA and PFOA at non-toxic and even environmentally relevant low doses in vitro. Cellular accumulation of TBBPA/PFOA was detected by UPLC-MS/ MS. Serum albumin binding constant of TBBPA or PFOA under single and co-existence was detected by fluorescence spectrometric titration, and the effects of varied albumin binding affinity on cellular accumulation were evaluated. Then, combined methods of transcriptomics, Q-PCR, Western blot, immunofluorescence imaging, gene knockdown and molecular docking were employed to detect epidermal growth factor receptor (EGFR) expression, internalization and its role in contributing to the cellular uptake of the pollutants. Results: Cell viability under co-exposure with 100 mu M TBBPA/250 mu M PFOA at non-toxic concentration alone reduced to 65.55 %, while the ratio of apoptotic and necrotic cells enhanced to 63.93 %. The combined toxicity was demonstrated to be synergism. Increased cellular accumulation of each pollutant was responsible for the synergistic toxicity. We next found TBBPA/PFOA co-existence can weaken each other's serum albumin binding ability, leading to higher free TBBPA and PFOA levels in medium that were easier for cellular uptake than albumin-bounded ones, thereby resulting in the enhanced cellular levels of both compounds. Endocytosis was then demonstrated to contribute to the cellular uptake of free TBBPA/PFOA molecules. Thereafter, a noncanonical EGFR internalization was activated and upregulated due to the cellular oxidative stress, which further mediated more cellular uptake of TBBPA/PFOA. Conclusion: Taken together, the effects of weakened serum albumin binding-to-activated EGFR internalization contributed to the enhanced cellular accumulation of each pollutant in a cascade mode, thereby resulting in the combined cytotoxicity. Our findings represent the first experimental study on BFRs and PFAS co-exposure risks with TBBPA/PFOA, and propose a new mechanism for the combined toxicity, which may have broad environmental, chemical, and biomedical significance for future research on the other environmental pollutants and their analogs.

Chlorophenols (CPs) are toxic pollutants widely present in the water environment. Yet their specific influence on gametogenesis remains unclear. This study investigated the impact of 2,4-dichlorophenol and pentachlorophenol on the gametogenesis of zebrafish. Results showed reduced egg production and sperm density in CP-exposed zebrafish, with an increase in the proportion of early germ cells and a decrease in mature germ cells. Additionally, the expression of gametogenesis-related genes (nanos3, ccnd1, dmc1) was upregulated, together confirming CPs suppress gametogenesis. The study also assessed the effects of CPs on sex hormone signaling, revealing altered ratios of estradiol to 11-ketotestosterone and changed expression of hormone receptors (esrs and ar). Besides, the hypothalamic-pituitary-gonadal axis genes showed significantly change, indicating the disorder of sex hormone signaling. Moreover, CPs increased DNA methylation levels in gonads, especially at CpG sites in the ar promoter, which negatively correlated with ar expression. Furthermore, elevated DNA methyltransferase (dnmts) expression was observed, and there was a significant interaction between CPs and Dnmts, suggesting CPs influence DNA methylation pathways. Overall, CPs inhibit gametogenesis by disrupting hormone signaling through DNA methylation. This study provides a new perspective on the toxic mechanisms and the risks posed by CPs to aquatic organisms.

Protein kinases are critical regulators of cellular functions and play a pivotal role in male reproduction. In this study, we investigated the role and regulatory mechanisms of the testis-specific serine/threonine kinase 6 (tssk6) in zebrafish. We found that tssk6 gene is highly expressed in the testis of adult male zebrafish, with its protein sequence showing high homology to those of mice and humans, highlighting its evolutionary conservation across vertebrates and suggesting an ancient, critical role in male reproduction. By constructing tssk6 mutants, we demonstrated that deletion of this gene leads to impaired testis development, reduced sperm quality, and decreased fertilization capacity in male zebrafish, directly linking tssk6 to the regulation of male fertility. In addition, transcriptome analysis of testis from tssk6 mutants further revealed significant changes in the expression of genes essential for spermatogenesis, sperm-egg recognition and fusion, shedding light on the molecular mechanisms underlying these reproductive defects. Collectively, these findings highlight the critical regulatory role of tssk6 in male zebrafish fertility. Our study not only advances our understanding of the molecular mechanisms underlying male reproduction but also provides valuable insights into conserved reproductive pathways in vertebrates.

Understanding genetic diversity is essential for conserving and sustainably managing fish populations in riverine ecosystems. However, overexploitation, habitat degradation, pollution, and ineffective fisheries management threaten the genetic integrity of many species, including the bagrid catfish (Rita rita). This study used simple sequence repeat (SSR) markers to assess the genetic diversity and population structure of R. rita across five sites along the Indus River. Genomic DNA was extracted from dorsal muscle tissues, and cross-species microsatellite primers from Bagarius yarrelli were used for polymerase chain reaction (PCR) amplification. Genetic diversity was evaluated using allelic richness (Ar), heterozygosity, inbreeding coefficients (F IS) and genetic differentiation (F ST). The results revealed moderate genetic diversity, with allelic richness ranging from 2.400 to 5.800 and expected heterozygosity (He) between 0.617 and 0.699. Lower observed heterozygosity (Ho) across most populations suggests potential inbreeding effects. Significant genetic differentiation (F ST) indicated moderate population structuring, with a strong correlation between geographic distance and genetic variation. Analysis of molecular variance (AMOVA) showed that 85.72% of genetic variation occurred within individuals, while restricted gene flow (Nm) across certain loci suggested geographical barriers affect genetic diversity. UPGMA clustering and STRUCTURE analysis identified two major genetic clusters, suggesting the presence of distinct evolutionary lineages. These findings highlight the need for targeted conservation strategies to maintain genetic integrity and reduce further genetic loss. This study establishes a molecular framework for future marker-assisted conservation and aquaculture programs to sustain R. rita populations in their natural habitats.

Targeting ferroptosis, a type of cell death elicited by Fe2+ and lipid reactive oxygen species (L-ROS), provides a novel strategy for cancer therapy. Selenium has the potential to treat cancers by acting as a pro-oxidative agent, thus leading to cancer cell death. Here, we found that the triple negative breast cancer (TNBC) MDA-MB-231 cells were more sensitive to ferroptosis induced by sodium selenite (Na2SeO3) than that of non-TNBC MCF-7 cells. Na2SeO3 significantly elevated the level of L-ROS, MDA and Fe2+, decreased the content of GSH and the enzyme activity of GPx, disrupted the expression of ferroptosis related proteins such as GPx4 and FTH1, as well as compromised mitochondrial morphology in MDA-MB-231 cells. Moreover, ATM was activated by Na2SeO3 in MDA-MB-231 cells. Notably, Na2SeO3-induced ferroptosis was inhibited by ATM kinase inhibitor KU55933 or siATM, suggesting that Na2SeO3-induced ferroptosis was mediated by ATM protein in MDA-MB-231 cells. Our findings suggest a therapeutic strategy by ferroptosis against TNBC and deepened our understanding of ATM function.

The combined pollution of lead (Pb) and polystyrene microplastics (PS-MPs) is common in aquatic environments. However, the combined neurotoxicity of these two pollutants is still poorly understood. In this study, zebrafish (Danio rerio) larvae were used to assess the combined neurotoxicity and mechanism of Pb and PS-MPs at environmentally relevant concentrations. The results showed that Pb (10 μg/L) induced abnormal behavior including significantly reduced movement distance, maximum acceleration, and average velocity (P < 0.05) along with altered expression of neurodevelopment-related genes (gap43 and α1-tubulin) (P < 0.05). PS-MPs (25 μg/L, 250 μg/L; diameter at 25 μm) co-exposure not only significantly reduced the concentration of Pb in the exposed solution (P < 0.01), but also decreased the uptake of Pb by downregulating the divalent metal transporter 1 gene (dmt1) (P < 0.01), thereby alleviating Pb-induced neurotoxicity. However, to demonstrate that PS-MPs alleviate the neurotoxicity of Pb by reducing Pb uptake, upregulation of dmt1 by addition of deferoxamine (DFO, an efficient iron chelator, 100 μM) significantly increased the Pb uptake and exacerbated neurotoxicity in zebrafish. In summary, our results demonstrated that PS-MPs alleviate Pb neurotoxicity by downregulating the mRNA level of dmt1 and decreasing the Pb uptake. This study provides a new insight into the combined neurotoxicity and underlying mechanisms of PS-MPs and Pb on zebrafish.

Diethylhexyl phthalate (DEHP) is a typical environmental pollutant and poses a potential threat to organisms by disrupting the lipid metabolism. This study found that DEHP at environmental concentrations, led to lipid accumulation in female zebrafish, as indicated by significant increases in the content of total cholesterol, triglycerides and the lipid droplets, in a concentration-dependent manner. However, how DEHP induces the lipid accumulation remains poorly understood. Our results demonstrated that DEHP up-regulated the expression of fat synthesis related-genes fas, acc, acs, elvol6, scd and dgat1, and increased the enzymatic activity of fatty acid synthase and acetyl-CoA carboxylase. Furthermore, the expression of several key transcription factors that regulate fat synthesis was detected, among which active sterol regulatory element-binding protein-1 (SREBP-1) was significantly increased. When active SREBP-1 was inhibited with specific inhibitor or knocked down by transient transfection, the expression of lipid synthesis-related genes was significantly decreased in DEHP group, indicating that DEHP disrupted the lipid synthesis via SREBP-1 pathway. Additionally, molecular docking revealed direct interaction sites between DEHP and SREBP-1. Our findings revealed that DEHP could directly activate SREBP-1-mediated lipid synthesis, providing theoretical basis for DEHP threatening biological health.

Previous studies have reported the feminizing effects of 2,4-dichlorophenol (2,4-DCP) on zebrafish (Danio rerio). However, the effect of 2,4-DCP on the number of primordial germ cells (PGCs), an indicator for early sex differentiation, remains elusive. In the present study, Tg (piwil1:egfp-UTR nanos3) zebrafish (GFP-labeled PGCs) were treated with 2,4-DCP (10, 20, and 40 μg/L) from 5 to 15 days postfertilization to explore the effect on PGC numbers and to elucidate associated molecular mechanisms. The results showed that 2,4-DCP exposure increased PGC numbers, as evidenced by larger GFP fluorescent areas, upregulated expressions of PGC marker genes (vasa and dnd), and raised the female ratio. Notably, the mRNA level of estrogen receptor 2a (esr2a) was also increased subsequently. Moreover, docking studies revealed stable 2,4-DCP interactions with ESR2a, speculating a role of ESR2a signaling pathway in 2,4-DCP toxicity. Furthermore, in esr2a knockout (esr2a-/-) zebrafish, the effects of 2,4-DCP were considerably minimized, proving the involvement of the ESR2a signaling pathway in the 2,4-DCP-mediated increase in PGC numbers. Dual-luciferase reporter gene assay and point mutation studies demonstrated that 2,4-DCP-stimulated promoter activity was mediated by estrogen response element (ERE) located in -686/-674 of the vasa promoter and -731/-719 of the dnd promoter. Overall, 2,4-DCP can potentially enhance the expression of vasa and dnd by binding to zebrafish ESR2a, thus leading to increased PGC numbers and subsequent female-biased sex differentiation.

Lysosomal polarity changes have been reported to be able to reflect cell status in physiological and pathological processes, and may serve as a ubiquitous marker for cancer detection. Thus, to monitor polarity in lysosome is of great importance to distinguish abnormal cells in cell biology and oncologic pathology. Herein, a lysosometargeted and near-infrared (NIR) emissive probe, named DCM-ML, was found to be highly sensitive toward polarity, with fluorescence intensity exhibiting a linearly ratiometric relationship (I655/I705) against polarity (Delta f). The potential of DCM-ML for polarity detection has been successfully demonstrated in physiological and pathological processes in both cells and zebrafish. It was found that lysosomal polarity in cancer cells (HeLa, MCF-7 and HepG2) was lower than that in normal cells (LO2), and it would be gradually decreasing with the cell damage getting worse; while in contrast, lysosomal polarity increased gradually in autophagy process. Moreover, lysosomal polarity changes in zebrafish development were successfully monitored for the first time with the NIR ratiometric probe, which exhibited a gradually increasing trend during the development process. And polarity in live embryos and larvae was also found to be higher than that in dead ones. All the results demonstrate that DCM-ML has the potential application for cancer cell diagnosis, dead cell identification, and real-time monitoring of autophagy and zebrafish development processes by imaging of lysosomal polarity. The development of the probe should be helpful for studying lysosome-related physiological and pathological processes.

Cadmium (Cd) at low concentrations has a potential to promote cell proliferation. However, the molecular mechanisms of Cd-induced proliferation are not well understood. Here, we reported that Cd (0-500 nM) significantly promoted the proliferation of HepG2 cells as demonstrated by elevated cell viability, more EdU-positive cells and increased gene expression of KI-67 and COX-2. Meanwhile, the gene expression of DNA methyltransferases was found to be elevated while that of tumor suppressor genes DAPK1 and RASSF1A were decreased under Cd exposure. Correspondingly, the methylation level of promoters in DAPK1 and RASSF1A were increased. Specifically, the CpG sites at -461 (Chr3:50, 374, 481) of RASSF1A promoter, and that at -260 (Chr9:90, 113, 207), -239 (Chr9:90, 113, 228), and -68 (Chr9:90, 113, 399) of DAPK1 promoter, were significantly hypermethylated. Moreover, 5-azacytidine (an inhibitor of DNA methyltransferase) partly impaired Cd-induced promoter hypermethylation of RASSF1A and DAPK1 genes, increased their expressions and slowed down Cd-induced cell proliferation, suggesting that DNA methylation play an essential part in Cd-boosted proliferation. The study showed that Cd caused promoter hypermethylation of RASSF1A and DAPK1, decreasing their expression and leading to higher level of cell proliferation. Furthermore, Cd at low concentrations could influence DNA methylation, which may serve as the proliferative mechanism of Cd.

Previous study showed that lead (Pb) could induce ATM-dependent mitophagy. However, whether Pb has any impact on mitochondrial fusion and fission, the upstream events of mitophagy, and how ATM connects to these processes remain unclear. In this study, we found that Pb can disrupt mitochondrial network morphology as indicated by increased percentage of shortened mitochondria and by decreased mitochondrial footprints. Correspondingly, the expression of fission protein Drp1 and its association with mitochondrial marker Hsp60 were significantly increased, while those of fusion proteins Mfn2 and Opa1 and their co-localization with Hsp60 were drastically attenuated. Notably, the expression of p-Drp1 (Ser616) and its translocation to mitochondria were dramatically elevated. Moreover, a small amount of ATM could be detected in the cytoplasm around mitochondria in response to Pb, and the co-localization of p-ATM (Ser1981) with Drp1 and p-Drp1 (Ser616) was obviously increased while its co-localization with Mfn2 and Opa1 was dramatically decreased. Furthermore, siRNA silencing of ATM evidently promoted greater fission in response to Pb stress, indicating that ATM is involved in mitochondrial fragmentation. Our results suggest that cytoplasmic ATM is an important regulator of Pb-induced mitochondrial fission.

Human serum albumin (HSA), as the most abundant protein in blood plasma, plays a crucial role in many physiological processes. The abnormal HSA level in serum or in urine is often associated with various diseases. Therefore, to achieve highly sensitive and selective quantification of HSA is of great importance for disease diagnosis and preventive medicine. Herein, an HSA-selective light-up fluorescent sensor, DCM-ML, was successfully developed for quantitative detection of HSA. DCM-ML exhibited good (photo-) stability and strong fluorescence enhancement around 630 nm in the presence of HSA in complex samples containing numerous biological analytes. Upon addition of HSA into DCM-ML containing solution, a good linear relationship (R2 > 0.99) between the fluorescence intensity of DCM-ML and HSA concentration from 0 to 0.08 mg/mL was obtained with the detection limit of 0.25 μg/mL. The sensing mechanism of the sensor towards HSA was demonstrated to be via recognition in the fatty acid site 1 (FA1), instead of the most reported binding sites (Sudlow I and II) in HSA, for the first time, by both the displacement experiments and molecular docking simulation. Thus, DCM-ML can also be assumed as a potential FA1 site-binding marker for examining drugs binding to the FA1 site in HSA. At last, the utilization of sensor DCM-ML for quantification and validation of HSA in urine samples and cell culture medium was effectively demonstrated. Therefore, the development of DCM-ML should find great application potentials in the fields of analytical chemistry and clinical medicine as a highly sensitive HSA sensor.

2,4-Dichlorophenol (2,4-DCP), an estrogenic endocrine disruptor, is widely spread in aquatic environments and may interfere with normal physiological functions in fish. However, the influence of this chemical on the synthesis of sex hormones is not well understood. In the present study, zebrafish (Danio rerio) were exposed to 2,4DCP (80 and 160 mu g/L) with or without fadrozole (an aromatase inhibitor which inhibits the synthesis of estradiol) from 20 to 40 days post fertilization. Then, the sex ratio, the content of vitellogenin (VTG) and sex hormones (androstenedione (ASD), estrone (E1), 17 beta-estradiol (E2), estriol (E3), testosterone (T) and 11-ketotestosterone (11-KT)) were studied. Furthermore, the expression of genes involved in synthesis of sex hormones (cyp19a1a, cyp19a1b, 17 beta-hsd, 11 beta-hsd and cyp11b) along with the DNA methylation in cyp19a1a and cyp19a1b promoters was analyzed. The results showed that 2,4-DCP exposure led to female-biased ratio, increased the content of ASD, E2 and VTG, as well as the ratio of E2/11-KT, while decreased the levels of androgens (T and 11KT). The sex hormonal change can be explained by the significant up-regulation of cyp19a1a, cyp19a1b, 17 beta-hsd and 11 beta-hsd genes. In addition, hypomethylation of cyp19a1a promoter was involved in this process. Notably, fadrozole can partly attenuate 2,4-DCP-induced feminization, and recover the levels of ASD, E2 and 11-KT. Thus, these results demonstrate that 2,4-DCP induces feminization in fish by disrupting the synthesis of sex hormones.

Elevated temperature could influence the sex differentiation by altering the expression of sex-related genes in fish. However, the underlying mechanisms by which the gene expression is altered remain poorly understood. Here, we aimed to explore the role of DNA methylation in sex differentiation of zebrafish (Danio rerio) in response to elevated temperature. The results showed that high temperature (33°C) exposure of fish from 20 to 30 days post fertilization (dpf), compared to normal temperature (28°C), resulted in male-biased sex ratio and decreased expression of female-related genes including cyp19a1a, sox9b and esr1. Meanwhile, the expressions of DNA methyltransferases dnmt3a1 and dnmt3a2, and the DNA methylation levels in sox9b and esr1 promoter were significantly increased by high temperature, strongly implying that DNA methylation is involved in high temperature-induced masculinization of zebrafish. Co-treatment with 5-aza-2'-deoxycytidine (a DNA methylation inhibitor) attenuated the high temperature-induced masculinizing effect, recovered the expression of esr1 and sox9b, suppressed the transcription of dnmt3a1 and dnmt3a2, and decreased the methylation of esr1 and sox9b promoter, further confirming that DNA methylation plays an important role in high temperature-induced masculinization of zebrafish. Furthermore, the methylation of sox9b promoter decreased the enrichment of transcription factor CREB (cAMP-responsive element binding proteins). Overall, these findings suggest that high temperature induce masculinization of zebrafish by down-regulation of female-related genes via DNA methylation, providing a new insight in understanding the epigenetic mechanism of thermal-mediated sex differentiation in fish.

黄河兰州段水体中的污染物,随着灌溉进入农业生态系统,在水-土-生物-人体中迁移和富集,不仅给两岸的生态环境带来严重影响,还对动物植物造成各种损伤,甚至危害到人体健康.综述了在黄河兰州段污灌农业生态系统中的环境污染监测、生态风险评估及生态修复方面的工作进展,总结了存在的问题,提出了一些措施与对策.