ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
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2025
·
IF 6.1
Xin Wang,Jie Zhao,Zehong Wu,Ling Wang,Wenjuan Zhang,Jie Zhang,Yong Liang
Bisphenol M (BPM), a structural analog of bisphenol A (BPA) commonly used in food packaging and consumer plastics, remains incompletely characterized in terms of its obesogenic potential and underlying molecular mechanisms, posing challenges for evidence-based risk assessment. To address this gap, we investigated the obesogenic effects and metabolic impacts of BPM exposure in male BALB/c mice through integrated liver untargeted metabolomics and gut microbiome analysis. Our results showed that BPM exposure significantly increased body fat percentage, enlarged the epididymal white adipose tissue volume, and induced hepatic steatosis. Untargeted metabolomics revealed that BPM disrupted hepatic metabolic pathways, such as riboflavin metabolism, glycerophospholipid metabolism and fatty acid degradation. Concurrently, BPM altered gut microbiota, increasing the Firmicutes/Bacteroidetes ratio and abundances of Staphylococcus and Jeotgalicoccus . Correlation networks linked these microbial shifts to hepatic lipid metabolites, specifically implicating linoleic acid metabolism as a potential mediator of gut-liver crosstalk in obesity development. These findings indicate that BPM promotes adiposity through liver-gut crosstalk, advancing the understanding of obesogenic risks associated with BPA alternatives.
研究领域:
毒理学
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代谢研究
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微生物组学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF RADIOANALYTICAL AND NUCLEAR CHEMISTRY
·
2014
·Vol. 302
·期 1
·123-130
·
IF 1.415
Sun Zhi-Zhong,Wei Hong-Yuan,Wang Guan-Quan,Zhou Zhi-Jun,He Jia-Heng,Wang Jing,Luo Shun-Zhong
[ 131 I]-5,10,15,20-tetrakis(4-hydroxyphenyl)porphyrin and [ 131 I]-5-(4-aminophenyl)-10,15,20-triphenylporphyrin ( 131 I-TPPOH and 131 I-TPPNH 2 ) were prepared and their biodistribution properties were evaluated in normal Kunming (KM) mice and SMMC-7721 tumor-bearing BALB/c mice. The optimized labeling yields were 98 and 96 % for 131 I-TPPOH and 131 I-TPPNH 2 , respectively. They were stable in vitro saline and in vivo. Both compounds had a specific affinity to liver and lung, and mainly metabolized through liver. They showed a time-dependent accumulation and retainable characteristics in SMMC-7721 tumor. These results supported their potential value for targeted tumor therapy agents.
研究领域:
放射医学
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肿瘤学
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药理学
✓ 已验证
DOI
高影响因子
ENVIRONMENTAL POLLUTION
·
2025
·
IF 7.3
Minyi Huang,Wentao Huang,Renyan Duan,Yingfeng Huang,Yongqiang Xia
Baicalein has pharmacological functions, such as antioxidant and anti-inflammatory properties, and has been shown to alleviate damage to organs caused by environmental pollutants. However, the mechanism by which baicalein reduces the toxic effects of metals needs further research. This study used Pelophylax nigromaculatus tadpoles as a model to explore the toxicological effects of lead (Pb) on the gut-liver axis, and the mechanism by which baicalein alleviates lead toxicity. Analysis of the gut microbiota showed that baicalein alleviated abnormal changes in the gut microbiota following Pb exposure, mainly by increasing the abundance of beneficial bacterial genera, including Cetobacterium , Clostridioides , and Monoglobus . Liver metabolomics showed that compared to a natural recovery, baicalein treatment significantly increased the content of metabolites such as uridine, 17α-hydroxypregnenolone, niacin, and cucurbitacin E, and significantly reduced the content of metabolites such as linoleic, gluconic acid, and tetrahydrocortisone. These differential metabolites could be enriched in pathways such as pyrimidine metabolism, nicotinic acid and nicotinamide metabolism, and steroid hormone biosynthesis, which were beneficial for the treatment of liver injury. There was a significant correlation between the gut microbiota and the main differential metabolites in the liver with the addition of baicalein. The improvement of these metabolic pathways by baicalein is beneficial for the repair of the liver and intestines. Therefore, baicalein can increase the abundance of beneficial gut microbiota, improve liver metabolism, and thus reduce the damage of Pb exposure to the gut-liver axis.
研究领域:
环境毒理学
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药理学
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产品关联
DOI
PubMed
高影响因子
PHYTOTHERAPY RESEARCH
·
2025
·
IF 6.3
Minghao Fan,Yudi Jiang,Chao Cai,Zhe Wang,Lu Chen,Shumin Hu,Xin Zhang,Hua Yin,Zhonghua Qian,Shuli Huang,Jiachen Yang
Depression often develops in young individuals and is linked to complications like cognitive impairment. Conventional antidepressants show limited efficacy in restoring cognitive function and may cause adverse effects. Green tea, a safe and health-promoting beverage, offers various health benefits. This study investigated the effects of long-term green tea consumption on stress-induced depression-like behavior and mild cognitive impairment in animal models. We established a rodent model of mild depression and studied the effects of green tea on depression-like behavior and cognitive impairment through comprehensive evaluation, including behavioral assessments, neurotransmitter quantification, gene and protein expression analysis, blood metabolite profiling, and gut microbiota characterization. Results demonstrated significant improvements in mood, long-term memory, and sterol and glycerophospholipid metabolism. Green tea repaired the intestinal barrier and upregulated genes vital for tight junctions and mucin production. It also enhanced gut microbiota composition, reducing the Firmicutes-to-Bacteroidetes ratio and promoting beneficial bacteria such as NK4A136 , Muribaculum , and Gordonibacter . These microbiota changes improved liver lipid metabolism and alleviated depressive symptoms. Green tea effectively mitigates depression-like behavior and cognitive deficits by modulating the gut-liver-brain axis.
研究领域:
神经科学
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营养学
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微生物学
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产品关联
DOI
PubMed
高影响因子
AQUATIC TOXICOLOGY
·
2023
·
IF 4.5
Wenting Lin,Yingjun Qin,Xinying Wang,Mingluo Du,Yukai Wang,Xiaohui Chen,Yuan Ren
Due to clinical treatment and illegal use, psychoactive substances have been widely detected in the aquatic environment. In this study, we investigated the effects of the benzodiazepine drug flunitrazepam (FLZ) and its metabolite 7-aminoflunitrazepam (7-FLZ) on the gut-liver axis of zebrafish. Zebrafish were exposed to two concentrations of FLZ and 7-FLZ (0.05 and 1 μg/L) for 30 days. Results showed that both FLZ and 7-FLZ exposure altered the relative abundance of Proteobacteria at the phylum level, with significant differences observed at the genus level for pathogenic bacteria such as Paracoccus, Shewanella , and Aeromonas. Metabolomics results showed both exposures significantly interfered with nucleotide and amino acid metabolism. The imbalance of gut microbiota and metabolic disorder increased the level of malondialdehyde, which in turn heightened the permeability of the gut mucosal barrier. FLZ and 7-FLZ induced oxidative stress in the liver via the gut-liver axis, leading to decreased levels of glucose, total cholesterol, and triglyceride, as well as the down-regulation of glycolipid metabolism-related genes ( PPARα, PPARγ, FABP2, Fabp11, PFKFB3 , and LDHA ). Metabolomics results revealed that FLZ and 7-FLZ significantly affected the biosynthesis of amino acids and arginine, and other metabolic pathways such as nucleotide, nicotinate and nicotinamide, and purine in the liver. Our results unveiled the mechanisms behind the toxicological effects of psychoactive substances on the gut-liver axis, providing valuable data for ecological and environmental risk assessments.
研究领域:
环境科学
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毒理学
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微生物组学
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产品关联
DOI
PubMed
高影响因子
Frontiers in Microbiology
·
2022
·
IF 6.064
Wu Xiaoyan,Han Ziyi,Liu Bingnan,Yu Dongming,Sun Jing,Ge Liangpeng,Tang Wenjie,Liu Shaojuan
Methionine (Met) metabolism provides methyl groups for many important physiological processes and is implicated in multiple inflammatory diseases associated with the disrupted intestinal microbiota; nevertheless, whether intestinal microbiota determines Met metabolism in the host remains largely unknown. Here, we found that gut microbiota is responsible for host Met metabolism by using various animal models, including germ-free (GF) pigs and mice. Specifically, the Met levels are elevated in both GF pigs and GF mice that mainly metabolized to S-adenosine methionine (SAM) in the liver. Furthermore, antibiotic clearance experiments demonstrate that the loss of certain ampicillin- or neomycin-sensitive gut microbiota causes decreased Met in murine colon. Overall, our study suggests that gut microbiota mediates Met metabolism in the host and is a prospective target for the treatment of Met metabolism-related diseases.
研究领域:
微生物学
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代谢生物学
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医学
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DOI
PubMed
高影响因子
Scientific Reports
·
2025
·Vol. 15
·期 1
·1-15
·
IF 3.9
Huang Minyi,Zhang Yuhao,Xu Xiang,Duan Renyan,Yang Hui
Chlorothalonil is a widely used fungicide that has a negative effect on individual movement, but its impact pathway needs further refinement. Here, the effects of exposure to chlorothalonil on the locomotion behavior of Pelophylax nigromaculatus tadpoles (GS23) were measured at three different levels (0 µg/L, 10 µg/L, and 50 µg/L), and the possible pathways of its effects were analyzed from the gut-liver axis. Chlorothalonil exposure levels of 10 µg/L and 50 µg/L significantly reduced the average speed of P. nigromaculatus tadpoles by 26% and 32.7%, respectively, and significantly decreased the locomotor frequency by 27.1% and 58.6%, respectively. Gut microbiota analysis revealed chlorothalonil exposure significantly increased the abundance of Firmicutes , while significantly decreased the abundance of Actinobacteriota , Pseudomonas , and Rhodococcus . Metabolomics analysis identified that chlorothalonil treatment changed amino acid-related metabolism pathways in the gut and liver and altered the glycerophospholipid metabolism pathway in the liver. This study indicated that chlorothalonil can affect individual locomotor abilities and interfering with the gut-liver axis of aquatic animals. These findings establish that chlorothalonil compromises aquatic organism motility through a multi-target mechanism involving gut microbiota modulation, amino acid metabolic interference, and hepatic lipid pathway disruption.
研究领域:
生态毒理学
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微生物组学
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代谢组学
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产品关联
DOI
PubMed
高影响因子
DRUG METABOLISM AND DISPOSITION
·
2018
·Vol. 46
·期 11
·1538-1545
·
IF 3.64
Jiangming Deng,Lianxia Guo,Baojian Wu
Human CYP2A6 (Cyp2a5 in mice) plays an important role in metabolism and detoxification of various drugs and chemicals. Here, we investigated a potential role of peroxisome proliferator-activated receptor γ (Ppar-γ) in circadian regulation of the Cyp2a5 enzyme. We first showed that Cyp2a5 mRNA and protein in mouse liver displayed robust circadian oscillations. Consistent with a circadian protein pattern, Cyp2a5-mediated 7-hydroxylation of coumarin was circadian time–dependent. Formation of 7-hydroxycoumarin was more extensive at a dosing time of Zeitgeber time 2 (ZT2) than that at ZT14. Interestingly, the nuclear receptor Ppar-γ was also a circadian gene. Circadian Ppar-γ protein level was strongly correlated with the Cyp2a5 mRNA level (r = 0.989). Furthermore, Ppar-γ activation (by a selective agonist, rosiglitazone) upregulated Cyp2a5 expression in Hepa-1c1c7 cells, whereas Ppar-γ knockdown downregulated Cyp2a5 expression. Also, Ppar-γ knockdown blunted the rhythmicity of Cyp2a5 mRNA in serum-shocked Hepa-1c1c7 cells. In addition, a combination of promoter truncation analysis, mobility shift, and chromatin immunoprecipitation assays revealed that Ppar-γ directly bound to a PPAR response element (i.e., the −1418- to −1396-bp region) within Cyp2a5 promoter and activated the gene transcription. Taken together, Ppar-γ was a transcriptional activator of Cyp2a5, and its rhythmic expression contributed to circadian expression of Cyp2a5.
研究领域:
药理学
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分子生物学
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昼夜节律生物学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2025
·
IF 8.5
Minghao Fan,Yudi Jiang,Chao Cai,Zhe Wang,Lu Chen,Xin Zhang,Hua Yin,Shumin Hu,Jia Liu,Zhonghua Qian,Shuli Huang
Cognitive impairment associated with natural aging significantly reduces the healthy lifespan of elderly adults. Barley is rich in polysaccharides, particularly starch and dietary fibers such as β-glucan and xylan. As the predominant components of barley water extracts, these polysaccharides, especially dietary fibers, exhibit substantial potential in promoting gut and brain health. In this study, we established a natural aging model by exposing mice to a high-fat diet and chronic stress for 220 consecutive days. Our findings revealed that barley polysaccharides ameliorated cognitive deficits, particularly long-term memory, by modulating neurotransmitter levels and reducing corticosterone. Barley polysaccharides also alleviated lipid metabolism disorders, reduced liver lesions, and decreased body weight as well as the percentage of visceral fat in mice by regulating bile acid and l -lysine metabolism. Additionally, barley polysaccharides enhanced intestinal barrier integrity and reshaped the gut microbiota. They significantly increased the abundance of norank_f_Muribaculaceae and unclassified f_Lachnospiraceae , leading to elevated short-chain fatty acid levels, especially butyric acid, which contributed to improved cognitive function. These findings suggest that barley polysaccharides could serve as a promising dietary intervention to mitigate cognitive decline associated with natural aging through the liver-gut-brain axis.
研究领域:
营养学
·
神经科学
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微生物学
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产品关联
DOI
PubMed
高影响因子
Scientific Reports
·
2025
·Vol. 15
·期 1
·1-23
·
IF 3.9
Sun Yuan-dong,Zhang Hao,Gong Xiao-long,Li Yuan-min,Han Ruiqin,Zhou Chun-xiao,Han Jian-jun
Metabolic Associated Fatty Liver Disease (MAFLD), previously known as Non-Alcoholic Fatty Liver Disease, is a growing global health issue associated with obesity, type 2 diabetes, and metabolic syndrome. This study investigates the potential of metformin, a common anti-diabetic drug, to slow the progression of MAFLD using a multi-omics approach. Male Wistar rats were fed a choline-deficient diet to induce MAFLD and treated with metformin through their drinking water for 48 weeks. We conducted a comprehensive analysis including liver histology, untargeted metabolomics, lipidomics, and gut microbiome profiling to assess the effects of metformin on liver and gut metabolic patterns. Metformin administration led to significant changes in gut microbiome diversity and the abundance of specific microbial species in MAFLD rats. Histological analysis showed that metformin-treated rats had reduced lipid accumulation and fibrosis in the liver compared to untreated MAFLD rats. Metabolomic and lipidomic analyses revealed that metformin corrected abnormal lipid metabolism patterns, reduced hepatic fat deposition, and influenced key metabolic pathways associated with MAFLD progression. Our findings suggest that metformin has a protective role against MAFLD by modulating gut microbiota and liver metabolism, thereby slowing the progression of hepatic fibrosis. This study provides insights into the therapeutic potential of metformin for MAFLD by addressing metabolic pattern disorders and abnormal changes in gut microbial diversity, highlighting its impact on lipid metabolism and gut-liver axis interactions.
研究领域:
生物医学
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微生物组学
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代谢组学
·
病理学
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产品关联
DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2024
·
IF 6.2
Jia-Meng Yang,Zhi-Hao Cao,Huo-Bin Tang,An-Ni Yang,Jia-Hui Liu,Jin-Hui Zhang,Hong-Liang Lu
Organophosphorus flame retardants, such as triphenyl phosphate (TPhP), exist ubiquitously in various environments owing to their widespread usage. Potential toxic effects of residual flame retardants on cultured non-fish species are not concerned commonly. TPhP-induced physiological and biochemical effects in an aquatic turtle were evaluated here by systematically investigating the changes in growth and locomotor performance, hepatic antioxidant ability and metabolite, and intestinal microbiota composition of turtle hatchlings after exposure to different TPhP concentrations. Reduced locomotor ability and antioxidant activity were only observed in the highest concentration group. Several metabolic perturbations that involved in amino acid, energy and nucleotide metabolism, in exposed turtles were revealed by metabolite profiles. No significant among-group difference in intestinal bacterial diversity was observed, but the composition was changed markedly in exposed turtles. Increased relative abundances of some bacterial genera (e.g., Staphylococcus , Vogesella and Lawsonella ) probably indicated adverse outcomes of TPhP exposure. Despite having only limited impacts of exposure at environmentally relevant levels, our results revealed potential ecotoxicological risks of residual TPhP for aquatic turtles considering TPhP-induced metabolic perturbations and intestinal bacterial changes.
研究领域:
生态毒理学
·
环境科学
·
水生生物学
✓ 已验证
DOI
PubMed
高影响因子
Environmental Chemistry and Ecotoxicology
·
2025
·
IF 8.2
Julong Wang,Yan Gao,Shanshan Yao,Lang Lin,Hengxiang Li,Shan Liu,Rui Hou,Zhijian Jiang,Xiangrong Xu
This study explores the impact of microplastics (MPs) and nanoplastics (NPs) on hepatic lipid metabolism in pearl gentian grouper ( Epinephelus fuscoguttatus ♀ × Epinephelus lanceolatus ♂) during overwintering and elucidates the underlying mechanisms. Fish were exposed to polystyrene (PS) MPs and NPs of varying sizes (5 μm, 500 nm, and 50 nm) for a 15-day exposure period. Histopathological analysis, oxidative stress assessment, and gene expression profiling related to lipid metabolism revealed significant toxic effects on the liver. Results showed that NPs preferentially accumulated in the liver, causing hepatocyte swelling, inflammation, and lipid metabolism disorders. Smaller particle sizes intensified oxidative stress, reduced triglyceride (TG) content, and elevated low-density lipoprotein cholesterol (LDL-C) and total cholesterol (T-CHO) levels. Transcriptomic analysis indicated that MPs and NPs altered the expression of lipid metabolism genes, particularly those in glyceride metabolism and lipolysis pathways, with significant upregulation of PNPLA2 and LIPG ( p < 0.05) under cold stress. This led to excessive energy reserve depletion and hepatic lipid metabolism dysfunction. This study establishes a “environmental stress-gene-metabolism” response model and provides novel insights into the molecular mechanisms by which NPs disrupt lipid homeostasis in aquatic organisms, offering a theoretical basis for understanding the toxicological effects of emerging contaminants.
研究领域:
环境毒理学
·
水产生物学
·
分子生态学
·
脂质代谢
·
应激生理学
✓ 已验证
产品关联
DOI
高影响因子
危险品化学品经营许可证（带存储）