Journal of Environmental Sciences
·
2026
·
IF 6.5
Xiaoyu Zhu,Yahui Shang,Heng Ni,Yuwei Wang,Chuang Ban,Zhenyan Cui,Sitong Dong,Yu Shi,Dajing Xia,Yihua Wu
DCOIT (4,5-dichloro-2-n-octyl-4-isothiazolin-3-one) is an antifouling biocide widely used as an alternative to organotin compounds. While previous studies had focused on its effects on energy production, endocrine disruption, and lipid metabolism, its impact on aging and underlying mechanisms remained unclear. Here, we demonstrated that environmentally relevant concentrations of DCOIT (37, 370 and 3700 ng/L) significantly impaired both lifespan and healthspan in Caenorhabditis elegans . RNA-seq and validation assays revealed that DCOIT upregulated comt-4 , a key gene in dopamine metabolism, leading to dopamine depletion and subsequent induction of oxidative stress. This redox imbalance critically contributed to accelerated aging phenotypes. Importantly, both genetic ( comt-4 RNAi) and pharmacological (opicapone) interventions restored dopamine levels, alleviated oxidative stress, and reversed DCOIT-induced aging deficits. Our study established the comt-4 /dopamine/oxidative stress axis as a central mechanism in DCOIT toxicity, suggesting dopamine modulation as a potential countermeasure against environmental toxicant-induced aging.
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ENVIRONMENTAL MONITORING AND ASSESSMENT
·
2023
·Vol. 195
·期 6
·1-15
·
IF 3
Wang Yan,Han Xue,Zhang Jie,Zhou Meng-Xuan,Liu Ai-Lin
Biological effect-based monitoring is essential for predicting or alerting to a possible deterioration in drinking water quality. In the present study, a reporter gene assay based on oxidative stress–mediated Pgst-4::GFP induction in the Caenorhabditis elegans strain VP596 (VP596 assay) was assessed for its applicability in evaluating drinking water safety and quality. This assay was used to measure the oxidative stress response in VP596 worms exposed to six ubiquitous components (As 3+ , Al 3+ , F − , NO 3 − -N, CHCl 3 , and residual chlorine) in drinking water, eight mixtures of these six components designed through orthogonal design, ninety-six unconcentrated water samples from source to tap water in two supply systems, and organic extracts (OEs) of twenty-five selected water samples. Pgst-4::GFP fluorescence was not induced by Al 3+ , F − , NO 3 − -N, and CHCl 3 , and was significantly enhanced by As 3+ and residual chlorine only at concentrations higher than their respective drinking water guideline levels. Pgst-4::GFP induction was not detected in any of the six-component mixtures. Induction of Pgst-4::GFP was observed in 9.4% (3/32) of the source water samples but not in the drinking water samples. However, a notable induction effect was revealed in the three OEs of drinking water, with a relative enrichment factor of 200. These results suggest that the VP596 assay has limited utility for screening drinking water safety by testing unconcentrated water samples; however, it offers a supplemental in vivo tool for prioritizing water samples for an enhanced quality assessment, monitoring pollutant removal performance by drinking water treatment plants, and evaluating water quality in water supplies.
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MOLECULES
·
2023
·Vol. 28
·期 17
·6303
·
IF 4.6
Chuhong Chen,Ying Deng,Linyan Liu,Zhenyan Zou,Chenzhong Jin,Zhiyin Chen,Shuanghui Wang
Deltamethrin (DM), a Type II pyrethroid, is widely used worldwide in agriculture, household applications, and medicine. Recent studies have shown that DM exerts a variety of toxic effects on organs such as the kidney, heart muscle, and nerves in animals. However, little is known about the effects of high-dose DM on growth and development, and the mechanism of toxicity remains unclear. Using theCaenorhabditis elegansmodel, we found that high-dose DM caused a delay in nematode development. Our results showed that high-dose DM reduced the activation of the endoplasmic reticulum unfolded protein response (UPRER). Further studies revealed that high-dose DM-induced developmental toxicity and reduced capacity for UPRERactivation were associated with the IRE-1/XBP-1 pathway. Our results provide new evidence for the developmental toxicity of DM and new insights into the mechanism of DM toxicity.Keywords:deltamethrin;Caenorhabditis elegans;development;toxicity;endoplasmic reticulum unfolded protein response
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ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
·
2023
·Vol. 30
·期 36
·85578-85591
·
IF 5.8
Tang Jielin,Qin Jinyan,Kuerban Guzailinuer,Li Jiayi,Zhou Qinyu,Zhang Hongdan,Sun Rongli,Yin Lihong,Pu Yuepu,Zhang Juan
As an emerging flame retardant, organic phosphate flame retardants have been extensively used worldwide. The aim of this study is to determine the effects of TnBP on neurobehavior of Caenorhabditis elegans ( C. elegans ) and its mechanisms. L1 larvae of wild-type nematodes (N2) were exposed to TnBP of 0, 0.1, 1, 10, and 20 mg/L for 72 hours. Then, we observed that the body length and body width were inhibited, the head swings were increased, the pump contractions and chemical trend index were reduced, the production of reactive oxygen species (ROS) was increased, and the expression of mitochondrial oxidative stress related genes ( mev-1 and gas-1 ) and P38 MAPK signal pathway-related genes ( pmk-1 , sek-1 , and nsy-1 ) was altered. After reporter gene strains BZ555, DA1240, and EG1285 were exposed to TnBP of 0, 0.1, 1, 10, and 20 mg/L for 72 hours, the synthesis of dopamine, glutamate, and Gamma-Amino Butyric Acid (GABA) was increased. In addition, the pmk-1 mutants (KU25) led to the sensitivity of C. elegans to TnBP in terms of head swings. The results showed that TnBP had harmful effects on the neurobehavior of C. elegans , oxidative stress might be one of the mechanisms of its neurotoxicity, and P38 MAPK signal pathway might play an important regulatory role in this process. The results revealed the potential adverse effects of TnBP on the neurobehavior of C. elegans .
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ENVIRONMENTAL POLLUTION
·
2025
·
IF 7.3
Yi Wang,Wanxin Liu,Ziwei Chen,Kaixin Zheng,Xianliang Yi,Jiao Wang,Xiaochen Chen,Xianhua Liu
Soil worms are among the most abundant and functionally diverse soil animals. However, they have been largely overlooked in studies on microplastic (MP) toxicity. MPs and plant secondary metabolites (PSMs) are ubiquitous in soil due to plant litter decomposition and heavy MP contamination, inevitably interacting and exerting combined toxicity on soil organisms. However, little research has been conducted on their joint effects. This study investigates the individual and combined toxic effects of polyethylene (PE) MPs and three PSMs (glycyrrhizic acid, tannic acid, and matrine) on the model organism Caenorhabditis elegans . Physiological and biochemical responses were assessed using fluorescence microscopy, image analysis, and statistical methods. After 42 h of exposure to PE MPs and/or PSMs, worm growth and development were negatively impacted. Under experimental conditions, matrine and PE MPs synergistically inhibited worm growth, exacerbated neurological damage, and induced oxidative stress. In contrast, glycyrrhizic acid and tannic acid alleviated PE MP-induced growth inhibition, mitigated oxidative stress, and demonstrated antioxidant properties that counteracted oxidative damage. This study offers new insights into the combined effects of MPs and PSMs in soil ecosystems, contributing to ecological risk assessments and pollution management strategies.
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FREE RADICAL BIOLOGY AND MEDICINE
·
2024
·
IF 7.1
Yiming Zhou,Mengting Zhang,Siyu Lu,Li Liu,Zhigui Duan,Fang Wei,Guolin Li
Purpose While reactive oxygen species (ROS) have been identified as key redox signaling agents contributing to aging process, which and how specific oxidants trigger healthy longevity remain unclear. This paper aimed to explore the precise role and signaling mechanism of superoxide (O 2 •− ) in health and longevity. Methods A tool for precise regulation of O 2 •− levels in vivo was developed based on the inhibition of superoxide dismutase 1 (SOD1) by tetrathiomolybdate (TM) in Caenorhabditis elegans ( C. elegans ). Then, we examined the effects of TM on lifespan, reproduction, lipofuscin accumulation, mobility, and stress resistance. Finally, the signaling mechanism for longevity induced by TM-O 2 •− was screened by transcriptome analysis and tested in sod-1 and argk-1 RNAi strains, sod-2 , sod-3 , and daf-16 mutants. Results TM promoted longevity in C. elegans with a concomitant extension of healthy lifespan as indicated by increasing fertility and mobility and reducing lipofuscin accumulation, as well as enhanced resistance to different abiotic stresses. Mechanically, TM could precisely regulate O 2 •− levels in nematodes via modulating SOD1 activity. An O 2 •− scavenger Mn(III)TBAP abolished TM-induced lifespan extension, while an O 2 •− generator paraquat at low concentration mimicked the life prolongation effects. The longevity in TM-treated worms was abolished by sod-1 RNAi but was not affected in sod-2 or sod-3 mutants. Further transcriptome analysis revealed arginine kinase ARGK-1 and its downstream insulin/insulin-like growth factor 1 signaling (IIS) as potential effectors for TM-O 2 •‾ -induced longevity, and argk-1 RNAi or daf-16 mutant nullified the longevity. Conclusions These findings indicate that it is feasible to precisely control specific oxidant in vivo and O 2 •− orchestrates TM-induced health and longevity in C. elegans via ARGK-1-IIS axis.
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Journal of Functional Foods
·
2018
·
IF 3.47
Shiling Feng,Haoran Cheng,Zhou Xu,Ming Yuan,Yan Huang,Jinqiu Liao,Ruiwu Yang,Lijun Zhou,Chunbang Ding
Panax notoginseng is Traditional Chinese medicine and also a China Food and Drug Administration (CFDA) approved food additive. In present study, we used Caenorhabditis elegans model to illustrate stress resistance and lifespan extension effect of a polysaccharide fraction form P. notoginseng (MRP5). Our data showed that MRP5 could significantly increase survival rate and markedly decreased ROS level of C. elegans under oxidative stress . Moreover, MRP5 could reduce the level of carbonyl protein and malondialdehyde of BA17 strain and extend lifespan of wild-type worms. The mechanism study revealed that MRP5 was able to promote the nuclear localization of DAF-16 resulting in the activation of antioxidant enzymatic systems. We also observed that MRP5 increased lifespan of daf-16 loss-of function mutant, suggesting MRP5-prolonged lifespan partially required daf-16 gene. Overall, our results illustrated the potential utilization of MRP5 as a functional food ingredient to delay aging.
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JOURNAL OF HAZARDOUS MATERIALS
·
2019
·
IF 7.65
Zhuo Li,Zhenyang Yu,Changzheng Cui,Fangting Ai,Daqiang Yin
Increasing concerns are earned on the multigenerational hazards of antibiotics due to the connection between their mother-children transfer via cord blood and breast milk and obesity in the children. Currently, Caenorhabditis elegans was exposed to sulfamethoxazole (SMX) over 11 generations (F0–F10). Indicators of obesogenic effects and gene expressions were measured in each generation and also in T11 to T13 that were the offspring of F10. Biochemical analysis results showed that SMX stimulated fatty acids in most generations including T13. The stimulation was resulted from the balance between enzymes for fatty acid synthesis (e.g., fatty acid synthetase) and those for its consumption (e.g., fatty acid transport protein). Gene expression analysis demonstrated that the obesogenic effects of SMX involved peroxisome proliferator activated receptors (PPARs, e.g., nhr-49 ) and insulin/insulin-like signaling (IIS) pathways (e.g., ins-1 , daf-2 and daf-16 ). Further epigenetic analysis demonstrated that SMX caused 3-fold more H3K4me3 binding genes than the control in F10 and T13. In F10, the most significantly activated genes were in metabolic and biosynthetic processes of various lipids, nervous system and development. The different gene expressions in T13 from those in F10 involved development, growth, reproduction and responses to chemicals in addition to metabolic processes.
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BMC Pharmacology & Toxicology
·
2026
·Vol. 27
·期 1
·133
·
IF 3.5
Sun Jun-Tao,Zhao Qi,Ren Ying-Ying,Wang Tian-Yu,Qi Wen-Hua
Background Synthetic musk ketone (MK) is extensively used in perfumes, cosmetics, and detergents. Due to its high lipophilicity, persistence, and limited removal efficiency in wastewater treatment, MK has been detected in various environmental matrices and human tissues. However, the ecotoxicity of MK remains poorly characterized. This study aimed to systematically evaluate the toxicological effects of MK and elucidate its underlying mechanisms using Caenorhabditis elegans ( C. elegans ) as a model organism. Methods Wild-type C. elegans (strain N2) were exposed to MK at concentrations ranging from 0.4 to 20 mg/L for 24 h. Physiological endpoints including body size, locomotor activity, lifespan, and brood size were assessed. Biochemical markers comprising reactive oxygen species (ROS) levels and lipofuscin accumulation were quantified. Acute heat-stress tolerance was evaluated to assess stress resistance. Transcriptome sequencing (RNA-seq) and quantitative real-time PCR (qRT-PCR) were employed to investigate molecular mechanisms. Differential gene expression analysis was performed using DESeq2, and functional enrichment analyses were conducted for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Results MK exposure significantly and concentration-dependently reduced body length and width, locomotor activity (head thrash and body bend frequencies), brood size, and lifespan. Lipofuscin accumulation and intracellular ROS levels were markedly elevated. Acute heat-stress tolerance was significantly impaired. Transcriptomic analysis identified 159 differentially expressed genes (DEGs) at 2 mg/L MK (19 up-regulated, 140 down-regulated) and 136 DEGs at 20 mg/L MK (30 up-regulated, 106 down-regulated). Key DEGs included ugt-30 (detoxification), Y9C9A.16 (oxidation-reduction), msp-59 (spermatogenesis), and acdh-8 (lipid metabolism). GO enrichment revealed significant alterations in spermatogenesis, protein catabolism, and kinase activity. KEGG pathway analysis identified perturbations in sulfur metabolism, branched-chain amino acid metabolism, fatty acid metabolism, and apoptosis. Protein-protein interaction network analysis identified cyc-2.2 and acdh-8 as hub genes. Conclusions MK exposure induces multi-faceted toxicity in C. elegans , including developmental impairment, neurotoxicity, reproductive toxicity, accelerated aging, and diminished stress resilience. These adverse outcomes are strongly associated with oxidative stress, germline impairment, and disrupted lipid metabolism, suggesting that these pathways play central roles in MK-induced toxicity. Our findings indicate that environmental exposure to MK may pose significant toxicological risks to living organisms and warrant further assessment of its ecological and health impacts.
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JOURNAL OF HAZARDOUS MATERIALS
·
2022
·
IF 14.224
Chongli Shi,Chen Wang,Lingjun Zeng,Yi Peng,Yeyong Li,Haibin Hao,Yang Zheng,Chao Chen,Haibo Chen,Jin Zhang,Minghui Xiang,Yuan Huang,Hui Li
Triphenyl phosphate (TPHP) is a widely used aryl organophosphate flame retardant (OPFR) that has attracted attention due to its frequent detection in the environment and living organisms. To date, the reproductive toxicity of TPHP has been investigated in organisms, but its molecular mechanisms are not fully understood. Caenorhabditis elegans ( C. elegans ) is the ideal animal for the study of reproductive toxicity following environmental pollutants, with short generation times, intact reproductive structures, and hermaphroditic fertilization. This study aimed to explore the reproductive dysfunction and molecular mechanisms induced by TPHP exposure in C. elegans . Specifically, exposure to TPHP resulted in a reduction in the number of eggs laid and developing embryos in utero, an increase in the number of apoptotic gonadal cells, and germ cell cycle arrest. The JNK signaling pathway is a potential pathway inducing reproductive toxicity following TPHP exposure based on transcriptome sequencing (RNA-seq). Moreover, TPHP exposure induced down-regulation of vhp-1 and kgb-2 gene transcription levels, and the knockout of vhp-1 and kgb-2 in the mutant strains exhibited more severe toxicity in apoptotic gonad cells, embryos, and eggs developing in utero, suggesting that vhp-1 and kgb-2 genes play a crucial role in TPHP-induced reproductive toxicity. Our data provide convergent evidence showing that TPHP exposure results in reproductive dysfunction through the JNK signaling pathway and improve our understanding of the ecotoxicity and toxicological mechanisms of aryl-OPFRs.
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INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2022
·Vol. 23
·期 9
·5003
·
IF 6.208
Rui Guo,Gen Li,Leilei Lu,Shan Sun,Ting Liu,Mengsha Li,Yong Zheng,Albertha J. M. Walhout,Jun Wu,Huixin Li
Plasmids are mostly found in bacteria as extrachromosomal genetic elements and are widely used in genetic engineering. Exploring the mechanisms of plasmid–host interaction can provide crucial information for the application of plasmids in genetic engineering. However, many studies have generally focused on the influence of plasmids on their bacterial hosts, and the effects of plasmids on bacteria-feeding animals have not been explored in detail. Here, we use a “plasmid–bacteria–Caenorhabditis elegans” model to explore the impact of plasmids on their host bacteria and bacterivorous nematodes. First, the phenotypic responses ofC. eleganswere observed by feedingEscherichia coliOP50 harboring different types of plasmids. We found thatE. coliOP50 harboring plasmid pEX18Gm unexpectedly increases the fecundity ofC. elegans. Subsequently, we found that the plasmid pEX18Gm indirectly affectsC. elegansfecundity via bacterial metabolism. To explore the underlying regulatory mechanism, we performed bacterial RNA sequencing and performed in-depth analysis. We demonstrated that the plasmid pEX18Gm upregulates the transcription of methionine synthase genemetHin the bacteria, which results in an increase in methionine that supportsC. elegansfecundity. Additionally, we found that a pEX18Gm-induced increase inC. eleganscan occur in different bacterial species. Our findings highlight the plasmid–bacteria–C. elegansmodel to reveal the mechanism of plasmids’ effects on their host and provide a new pattern for systematically studying the interaction between plasmids and multi-species.Keywords:plasmid–host interaction;bacteria;C. elegans;fecundity;multi-species;RNA-seq;methionine;HPLC-MS/MS
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CHEMOSPHERE
·
2022
·
IF 8.943
Yunjiang Yu,Xin Hua,Haibo Chen,Yue Yang,Yao Dang,Mingdeng Xiang
Tetrachlorobisphenol A (TCBPA), an alternative to tetrabromobisphenol A (TBBPA), is ubiquitous in the environment and could potentially impact the reproductive system of organisms. However, the mechanisms underlying TCBPA-mediated reproductive effects remain unclear. Herein, we exposed Caenorhabditis elegans ( C. elegans , L4 larvae) to TCBPA at environmentally relevant doses (0–100 μg/L) for 24 h. Exposure to TCBPA at concentrations of 1–100 μg/L impaired fertility of C. elegans , as indicated by brood size . After staining, the number of germline cells decreased in a dose-dependent manner, whereas germline cell corpses increased in exposed nematodes (10–100 μg/L TCBPA). Moreover, the expression of genes related to the germline apoptosis pathway was regulated following exposure to 100 μg/L TCBPA, indicating the potential role of DNA damage in TCBPA-induced apoptosis. Apoptosis was nearly abolished in ced-4 and ced-3 mutants and blocked in hus-1 , egl-1 , cep-1 , and ced-9 mutants. Numerous foci were detected in TCBPA (100 μg/L)-exposed hus-1::GFP strains. These results indicate that TCBPA induces hus-1 -mediated DNA damage and further causes apoptosis via a cep-1 -dependent pathway. Our data provide evidence that TCBPA causes reproductive toxicity via DNA damage-induced apoptosis.
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