Toxics最新文献

{"title":"Effects of Environmental Non-Essential Toxic Heavy Metals on Epigenetics During Development.","authors":"Hisaka Kurita, Kazuki Ohuchi, Masatoshi Inden","doi":"10.3390/toxics13030167","DOIUrl":"10.3390/toxics13030167","url":null,"abstract":"<p><p>We are exposed to a variety of environmental chemicals in our daily lives. It is possible that the effects of this daily chemical exposure could accumulate in the organism in some form and influence health and disease development. The exposure effects extend throughout the human lifetime, not only after birth, but also during the embryonic period. Epigenetics is an important target for the molecular mechanisms of daily environmental chemical effects. Epigenetics is a mechanism of gene transcription regulation that does not involve changes in DNA sequence. The Developmental Origins of Health and Disease (DOHaD) theory has also been proposed, in which effects such as exposure to environmental chemicals during embryonic period are mediated by epigenetic changes, which may lead to risk for disease development and adverse health effects after maturity. This review summarizes the association between embryonic exposure and the epigenetics of well-known non-essential toxic heavy metals (methylmercury, cadmium, arsenic, and lead), a representative group of environmental chemicals. In the future, it will be important to predict the epigenetic mechanisms of unknown chemical and combined exposures. In addition, further experimental investigations using experimental animals and the accumulation of knowledge are needed to study the transgenerational effects of environmental chemicals in the future.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"13 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11946632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paternal DEHP Exposure Triggers Reproductive Toxicity in Offspring via Epigenetic Modification of H3K27me3.","authors":"Lu Zhang, Rui Yang, Guiyong Xu, Lingqiao Wang, Weiyan Chen, Yao Tan, Guowei Zhang, Wenbin Liu, Guanghui Zhang, Jun Li, Ziyuan Zhou","doi":"10.3390/toxics13030172","DOIUrl":"10.3390/toxics13030172","url":null,"abstract":"<p><p>Di (2-ethylhexyl) phthalate (DEHP) is an acknowledged endocrine disruptor with male reproductive toxicity; nevertheless, the transgenerational impacts on male offspring resulting from paternal exposure, along with the mechanisms involved, are not well understood. To develop a transgenerational model of DEHP paternal exposure, male C57BL/6J mice (4-week) exposed to DEHP (5, 250, and 500 mg/kg/d) for 35 days were then bred with unexposed female mice at a ratio of 1:2 to produce offspring. Findings indicate that the sperm quality and relative sex hormones were adversely affected in males of F1 and F2 generations, and pathological damage in the testes and the apoptosis of testicular cells were also observed. Interestingly, an increase in the expression levels of H3K27me3 was observed in the testicular tissues of male descendants. It was further confirmed by in vitro approach that H3K27me3 may down-regulate the expression of Bcl-2 and plays a role in regulating the initiation of apoptosis in Leydig cells triggered by MEHP (the primary metabolite of DEHP). Additionally, the down-regulation of Bcl-2 can be reversed by treatment with the H3K27me3 inhibitor GSK126. To conclude, DEHP leads to transgenerational harm to male offspring reproductive systems, with the epigenetic mechanism of H3K27me3 playing a key role in mediating these effects.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"13 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11945355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Per- and Polyfluoroalkyl Substances and All-Cause Mortality in Diabetic Patients: Insights from a National Cohort Study and Toxicogenomic Analysis.","authors":"Zhengxiao Wei, Jinyu Chen, Xue Mei, Yi Yu","doi":"10.3390/toxics13030168","DOIUrl":"10.3390/toxics13030168","url":null,"abstract":"<p><p>Per- and polyfluoroalkyl substances (PFAS) are a group of environmental contaminants associated with various health risks; however, their relationship with all-cause mortality in individuals with diabetes remains unclear. A total of 1256 participants from the National Health and Nutrition Examination Survey (NHANES) were included to explore the association between seven PFAS compounds and all-cause mortality in diabetic patients. Preliminary logistic regression identified three PFAS compounds (perfluorooctanoic acid [PFOA], perfluorooctane sulfonic acid [PFOS], and 2-(N-methyl-PFOSA) acetate acid [MPAH]) as significantly associated with mortality in the diabetic population. The optimal cut-off values for PFOS, PFOA, and MPAH were determined using the X-tile algorithm, and participants were categorized into high- and low-exposure groups. Kaplan-Meier survival curves and multivariable Cox proportional hazards regression models were used to assess the relationship between PFAS levels and mortality risk. The results showed that high levels of PFOS were significantly associated with increased all-cause mortality risk in diabetic patients (hazard ratio [HR]: 1.55, 95% confidence interval [CI]: 1.06-2.29), while PFOA and MPAH showed no significant associations. To explore mechanisms underlying the PFOS-mortality link, toxicogenomic analysis identified 95 overlapping genes associated with PFOS exposure and diabetes-related mortality using the Comparative Toxicogenomics Database (CTD) and GeneCards. Functional enrichment analysis revealed key biological processes, such as <i>glucose homeostasis</i> and <i>response to peptide hormone</i>, with pathways including the <i>longevity regulating pathway</i>, <i>apoptosis</i>, and <i>p53 signaling pathway</i>. Protein-protein interaction network analysis identified 10 hub genes, and PFOS was found to upregulate or downregulate their mRNA expression, protein activity, or protein expression, with notable effects on mRNA levels. These findings suggest that PFOS exposure contributes to increased mortality risk in diabetic patients through pathways related to glucose metabolism, apoptosis, and cellular signaling. Our study provides new insights into the association between PFAS and all-cause mortality in diabetes, highlighting the need for large-scale cohort studies and further in vivo and in vitro experiments to validate these findings.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"13 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11945897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Water Quality Criteria of Dieldrin for the Protection of Aquatic Organisms and Wildlife Using a Tissue Residue Approach.","authors":"Li Xie, Xuemei Li, Liangwen Bao, Yuexin Zhang, Hailei Su, Xuesong Liu, Fanfan Wang, Yuan Wei, Ningning Ji, Min Zhou","doi":"10.3390/toxics13030173","DOIUrl":"10.3390/toxics13030173","url":null,"abstract":"<p><p>Dieldrin is legacy organochlorine insecticide, which was listed in the Stockholm Convention because of its persistence, bioaccumulation and toxicity. However, it is still present in the environment and in organisms two decades after its ban. The current criteria used for risk assessment in China are based on acute toxicity data in water columns without considering the bioavailability and bioaccumulation, which accordingly lead to the under-protection of aquatic organisms and wildlife. In this study, the water quality criteria (WQC) for dieldrin were derived from a combination of tissue-based toxicity data and the bioaccumulation factor (BAF) to better protect aquatic ecosystems. The dieldrin residue data in surface water in China were obtained by literature review and the ecological risk was assessed using the quotient method. Combined with a BAF of 58,884.37 L/kg estimated by the model, the WQC were calculated as needing to be 3.86 and 1.4 ng/L to protect aquatic life and aquatic-dependent wildlife, respectively. The results of the risk assessment revealed the potential high risk posed by dieldrin bioaccumulation. This study provides scientific guidance for the determination of the water quality standard for dieldrin and to ensure the risk management of the aquatic environment in China.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"13 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11946317/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Exposure to Different Types of Microplastics on the Growth and Development of <i>Rana zhenhaiensis</i> Tadpoles.","authors":"Shimin Xiao, Hao Chen, Xiyao Gao, Xinni He, Rongzhou Jin, Yunqi Wei, Shuran Li, Lei Xie, Yongpu Zhang","doi":"10.3390/toxics13030165","DOIUrl":"10.3390/toxics13030165","url":null,"abstract":"<p><p>Microplastic (MP) pollution is a major environmental problem, but a comparative study of the toxicological effects of different MPs remains lacking. To explore the toxicological effects of three different microplastics, namely, polypropylene (PP), polystyrene (PS) and polyethylene (PE), Zhenhai brown frog (<i>Rana zhenhaiensis</i>) tadpoles were used as the model animal. The results showed that exposure to PE and PS significantly reduced the metamorphosis rate of the tadpoles. Compared with the control group, the body weight of tadpoles in all MP treatments was significantly reduced compared with that of the control group. In addition, exposure to PE reduced the body length and hind limb length of tadpoles. The number of pigment cells increased and intercellular spaces expanded in the liver tissues of tadpoles receiving PS and PE treatments. The composition and function of the intestinal microbiota in the PP treatment and control groups were similar, whereas between the PS treatment and control, they differed. Liver transcriptome sequencing revealed significant alterations in key genes associated with oxidative stress, energy metabolism, immune response, and apoptosis signaling pathways with PS treatment and PP treatment. In summary, MPs may have harmed tadpoles to varying degrees by interfering with related signaling pathways. The negative effects of PE and PS were greater than those of PP.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"13 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11945619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lentinan Alleviated PM2.5 Exposure-Induced Epithelial-Mesenchymal Transition in Pulmonary Epithelial Cells by Inhibiting the GARP/TGF-β/Smad Pathway.","authors":"Zhi Wang, Shiqing Xu, Bohao Bian, Zhida Hu, Feiyang Wu, Siqi Zhao, Xiaohui Wang, Li Wang, Teng Ma","doi":"10.3390/toxics13030166","DOIUrl":"10.3390/toxics13030166","url":null,"abstract":"<p><p>PM2.5 (fine particulate matter) is an air pollutant widely present in urban and industrial areas, which has emerged as a significant threat to human health. Specifically, long-term exposure to PM2.5 could lead to various lung diseases, including pulmonary fibrosis and Chronic Obstructive Pulmonary Disease (COPD). The Glycoprotein A Repetitions Predominant (GARP) protein, a key receptor and regulator for TGF-β1, has recently emerged as a vital cytokine in PM2.5-induced pulmonary pathological changes. As a membrane glycoprotein, GARP binds to TGF-β, keeping it in an active state. Herein, PM2.5 treatment upregulated GARP and promoted Epithelial-Mesenchymal Transition (EMT) via TGF-β/SMAD signaling pathway activation. Conversely, lentinan (a shiitake mushroom-derived polysaccharide) effectively reversed the PM2.5-induced GARP upregulation, alleviating EMT. This study elucidates the role of GARP in PM2.5-induced EMT through the TGF-β/SMAD pathway in pulmonary epithelial cells and discusses the therapeutic potential of lentinan.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"13 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11946725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Ovary as a Target Organ for New Generation Bisphenols Toxicity.","authors":"Paulina Głód, Joanna Smoleniec, Weronika Marynowicz, Justyna Gogola-Mruk, Anna Ptak","doi":"10.3390/toxics13030164","DOIUrl":"10.3390/toxics13030164","url":null,"abstract":"<p><p>Bisphenols (BPs) are a group of organic compounds used extensively in plastics, coatings, and epoxy resins; they have been of concern recently due to their endocrine-disrupting effects. Among these, bisphenol A (BPA) is the most studied. Regulatory measures, such as the ban on BPA use in baby bottles by the European Union and its restricted use in thermal paper, reflect the growing awareness of the health risks of BPA. To mitigate these risks, analogs such as bisphenol S (BPS), bisphenol F (BPF), and others (BPAF, BPAP, BPB, BPP, BPZ) have been developed as alternatives. Despite their intended safety, these analogs have been detected in environmental media, including indoor dust and thermal receipt paper, as well as in human biological samples. Studies report their presence in urine at levels comparable to BPA, with BPS and BPF found in 78% and 55% of samples, respectively. In addition, BPs have been found in human follicular fluid (FF) at concentrations that could exert some paracrine effects on ovarian function and reproductive health. With the increased global production of BPs, occupational exposure and environmental contamination also increase. This review summarizes what is currently known about the effects of BPs on the ovary and the mechanisms by which PBs exert ovarian toxicity, with a particular focus on oogenesis, folliculogenesis, and steroidogenesis. Further, this review emphasizes their influence on reproductive functions and the need for further biosafety evaluations.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"13 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11946734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Puerarin Attenuates the Cytotoxicity Effects of Bisphenol S in HT22 Cells by Regulating the BDNF/TrkB/CREB Signaling Pathway.","authors":"Meilin Qin, Xinxin Guo, Nuo Xu, Yan Su, Mengfen Pan, Zhengbao Zhang, Huaicai Zeng","doi":"10.3390/toxics13030162","DOIUrl":"10.3390/toxics13030162","url":null,"abstract":"<p><p>Bisphenol S (BPS) is a widespread environmental endocrine disrupter that can cause hepatotoxicity, neurotoxicity and negative effects on reproduction. Puerarin (PUE) has been found to have anti-inflammatory, antioxidant, and neuroprotective properties, however, its potential protective effects against BPS-induced neurotoxicity and the underlying mechanisms are still not fully understood. In this study, HT22 cells were exposed to different concentrations of BPS with or without PUE. Cell viability, apoptosis, oxidative damage, and the expression level of axon-injury-related genes and the BDNF/TrkB/CREB pathway were analyzed. The results showed that 40 μM to 180 μM BPS and 100 μM to 180 μM PUE significantly decreased the cell viability of HT22 cells, but in the 80 μM PUE group, the cell viability was higher than control group, and the ratio of 1.1. Meanwhile, BPS increased the production of ROS and MDA but decreased the GSH and SOD. However, supplementation with PUE was alleviated the oxidative damage. PUE also alleviated the apoptosis rate that induced by BPS. Additionally, BPS decreased the expression levels of mRNA and proteins of synaptic-related genes, but inhibited the expression levels of mRNA and proteins of the BDNF/TrkB/CREB signaling pathway. Interestingly, PUE was found to significantly recover the expression of synaptic related genes, but also upregulated the expression of the BDNF/TrkB/CREB pathway. In conclusion, our study proved that PUE can attenuate the neurotoxicity effect of bisphenol S, which related to oxidative damage in HT22 cells by regulating the BDNF/TrkB/CREB signaling pathway. This study is not only the first to demonstrate that PUE can mitigate BPS-induced neurotoxicity through oxidative stress modulation, but also provides a novel therapeutic approach involving the BDNF/TrkB/CREB pathway. These findings offer promising insights into natural-based strategies for protecting against environmental neurotoxins and provide a foundation for future therapeutic developments targeting BPS-induced neurotoxicity.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"13 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11945520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Occurrence of 5-Hydroxymethylfurfural, Acrylamide, 3-Monochloro-1,2-Propanoldiol and Melamine in Infant Formulas: What Do We Know About These Compounds?","authors":"Xóchitl Yanine Méndez-Alvarado, María Magdalena Eréndira González-Tello, Jorge Luis Chávez-Servín, Karina de la Torre-Carbot, Teresa García-Gasca, Diana Beatriz Rangel-Peniche, Roberto Augusto Ferriz-Martínez","doi":"10.3390/toxics13030161","DOIUrl":"10.3390/toxics13030161","url":null,"abstract":"<p><p>In the manufacture of infant formulas, from raw materials to the final product, the ingredients are subject to high temperatures which favor the formation of undesirable compounds, some of them from the Maillard reaction, such as 5-hydroxymethylfurfural (HMF) and acrylamide, and others from thermal processing, such as the compound 3-monochloro-1,2-propanoldiol (3-MCPD). Finally, there is also a risk that the product may be adulterated with undesirable components such as melamine and cyanuric acid. Due to the vulnerability of infants during the first stage of life, this review answers the main question: How much of these undesirable compounds are present in commercial infant formulas, and what do we know about them? Accordingly, the review is divided into three sections: (1) Maillard reaction products (HMF and acrylamide), (2) products contained in vegetable oils (3-MCPD), and (3) fraudulent and/or adulterant compounds (melamine and cyanuric acid). The objective is to report on the occurrence of HMF, acrylamide, 3-MCPD, melamine, and cyanuric acid in infant formulas in order to support more solid public health policies related to infant feeding. These undesirable compounds represent a risk to infants, possibly contributing to kidney and neurological damage and causing mutations that increase the development of childhood cancer. Therefore, it is necessary to promote breastfeeding and establish stricter controls, with scientific evidence on the effects of HMF, acrylamide, 3-MCPD, melamine, and cyanuric acid in infant formulas to reduce their short- and long-term effects on infants' health.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"13 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11946680/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Any Way the Wind Blows Does Really Matter in Lichen Response to Air Pollution from an Oil Refinery.","authors":"Maja Maslać Mikulec, Saša Likić, Oleg Antonić, Mirta Tkalec","doi":"10.3390/toxics13030160","DOIUrl":"10.3390/toxics13030160","url":null,"abstract":"<p><p>Lichens serve as effective bioindicators for air pollution studies, yet most biomonitoring research focuses primarily on the distance from pollution sources, often neglecting wind data that could elucidate the spread of airborne pollutants. In our previous study in Slavonski Brod, Croatia, we utilized data from a monitoring station, emphasizing the impact of meteorological conditions, particularly wind, on the dispersal of pollutants from a neighbouring oil refinery. To gain a deeper understanding of air pollution dynamics, here, we studied lichen vitality-measured through photochemical efficiency and photosynthetic pigments-alongside the metal (Ni, Zn, Cd, Pb) and non-metal (sulphur and nitrogen) content in native lichen species <i>Flavoparmelia caperata</i> across 17 plots within a 20 km radius of the refinery. Our analysis employed generalized linear models (GLMs) to incorporate various environmental predictors, including distance from the refinery, direction-specific wind speed and frequency, vegetation density, and the orientation of lichen samples with respect to north and the refinery. Findings show that pollution levels are significantly influenced, not only by distance but also by direction-specific wind patterns, underscoring the necessity of including these variables in future biomonitoring studies and highlighting a critical need for air quality management interventions.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"13 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11945780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}