JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL AND LIFE SCIENCES
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2013
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IF 2.487
Shanshan Zhu,Futao Hu,Ting Yang,Ning Gan,Daodong Pan,Yuting Cao,Dazhen Wu
Analysis of tributyltin chloride (TBT) in environmental samples, such as seawater, is important in order to evaluate the TBT contamination and accumulation in the trophic chain. The environmental impact of organotin compounds has been a particular focus of analytical studies. The present study reports the use of molecular imprinting technology coupled with liquid chromatography–tandem mass spectrometry (LC–MS/MS) to determine trace amounts of TBT in seawater and seafood (mussel tissue samples). The imprinted polymer was synthesized by a non-covalent free-radical approach using acrylamide (AM) as a monomer and TBT as a template molecule in acetonitrile solvent (polymerization media). The imprinted polymer synthesized by this approach exhibited good adsorptive capacity and allowed specific retention of TBT. Recoveries of TBT in seawater samples spiked with different TBT concentrations ranged from 67.2% to 81.1% with peak area precision (RSD) < 3.7%, and recoveries of TBT in mussel tissue samples ranged from 75.0% to 94.2% with RSD < 4.8%.
研究领域:
环境科学
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分析化学
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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
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2020
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IF 6.793
Jiapeng Jie,Ling Ling,Yuguo Yi,Liang Tao,Xin Liao,Pingshi Gao,Qian Xu,Weigao Zhang,Yuxin Chen,Jianfa Zhang,Dan Weng
Tributyltin (TBT), a bioaccumulative and persistent environmental pollutant, has been proposed as a metabolism disruptor and obesogen through targeting peroxisome proliferator-activated receptor gamma (PPARγ) receptor pathway. However, it remains unknown whether this biological effect occurs in macrophage, a cell type which cooperates closely with hepatocytes and adipocytes to regulate lipid metabolism . This study for the first time investigated the effect of TBT on PPARγ pathway in macrophages. Our results indicated that nanomolar levels of TBT was able to strongly activate PPARγ in human macrophages. TBT treatment also markedly increased the intracellular lipid accumulation, and enhanced the expression of lipid metabolism-related genes in macrophages, while these effects were all significantly down-regulated in PPARγ-deficient macrophages, confirming the involvement of PPARγ in TBT-induced lipogenesis. Next, a mouse model that C57BL/6 mice were orally exposed to TBT with the doses (250 and 500 μg/kg body weight) lower than NOAEL (no observed adverse effect level) was used to further investigate the in vivo mechanisms. And the in vivo results were consistent with cellular assays, confirming the induction of PPARγ and the increased expression of lipogenesis-regulating and lipid metabolism-related genes by TBT in vivo. In conclusion, this study not only provided the first evidence that TBT stimulated lipogenesis, activated PPARγ and related genes in human macrophages, but also provided insight into the mechanism of TBT-induced metabolism disturbance and obesity through targeting PPARγ via both in vitro cellular assays and in vivo animal models.
研究领域:
毒理学
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分子生物学
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细胞生物学
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环境科学
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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
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2020
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IF 6.793
Jing Zhan,Xiaoran Ma,Donghui Liu,Yiran Liang,Peize Li,Jingna Cui,Zhiqiang Zhou,Peng Wang
Tributyltin (TBT), an organotin compound once widely used in agriculture and industry, has been reported to induce obesity and endocrine disruption. Gut microbiota has a strong connection with the host’s physiology. Nevertheless, the influences of TBT exposure on gut microbiota and whether TBT-influenced gut microbiota is related to TBT-induced toxicity remain unclear. To fill these gaps, ICR (CD-1) mice were respectively exposed to TBT at NOEL (L-TBT) and tenfold NOEL (H-TBT) daily by gavage for 8 weeks in the current study. The results showed that TBT exposure significantly increased body weight as well as epididymal fat, and led to adipocyte hypertrophy, dyslipidemia and impaired glucose and insulin homeostasis in mice. Additionally, TBT exposure significantly decreased the levels of T4, T3 and testosterone in serum. Also of note, TBT exposure changed gut microbiota composition mainly by decreasing Bacteroidetes and increasing Firmicutes proportions. To confirm the role of gut microbiota in TBT-induced overweight and hormonal disorders, fecal microbiota transplantation was performed and the mice receiving gut microbiota from H-TBT mice had similar phenotypes with their donor mice including significant body weight and epididymal fat gain, glucose and insulin dysbiosis and hormonal disorders. These results suggested that gut microbiome altered by TBT exposure was involved in the TBT-induced increased body weight, impaired glucose and insulin homeostasis and endocrine disruption in mice, providing significant evidence and a novel perspective for better understanding the mechanism by which TBT induces toxicity.
研究领域:
毒理学
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微生物学
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内分泌学
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代谢学
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产品关联
DOI
PubMed
高影响因子
Environmental Sciences Europe
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2020
·Vol. 32
·期 1
·1-14
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IF 5.394
Wu Lingling,Chen Ling,Zhu Lingjiao,Chen Xiaoping,Li Qian
Sediments function as a secondary and significant source of tributyltin (TBT) and triphenyltin (TPT) in aquatic ecosystems and may pose a potential threat on benthic organisms and human health. The subchronic toxicity of sediment-associated TBT or TPT to snails Bellamya aeruginosa at environmentally relevant concentrations was investigated in this study. Multiple endpoints at the biochemical [ethoxyresorufin-O-deethylase (EROD), superoxide dismutase (SOD), catalase (CAT), protein carbonyl content (PCC) and lipid peroxidation (LPO)] and transcriptomic levels were examined.TBT or TPT in sediment could induce antioxidant enzymes’ activities and result in oxidative damage in the hepatopancreas of B. aeruginosa after 28-day exposure. A transcriptomic profile of B. aeruginosa exposed to TBT and TPT was reported. CYP genes and EROD activity were sensible and reliable biomarkers for toxicity assessment of TBT or TPT in sediments. Comparative pathway analysis revealed the alteration of steroid hormone biosynthesis and retinol metabolism in B. aeruginosa after 90-day exposure to sediment-associated TBT at the concentration of 2000 ng/g dw, which might affect both reproduction and lipogenesis functions. The ubiquitin proteasome system and immune system might be the toxicity target in B. aeruginosa after exposure to sediment-associated TPT for 90 days.The results offered new mechanisms underlying the toxicity of sediment-associated tributyltin and triphenyltin.
研究领域:
环境毒理学
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分子生物学
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生态毒理学
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水生科学
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DOI
高影响因子
ENVIRONMENTAL RESEARCH
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2024
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IF 7.7
Jianjun Chen,Yinyin Wei,Jiameng Zhou,Xianglin Cao,Rongjie Yuan,Yaoyajie Lu,Yi Guo,Xue Shao,Weidi Sun,Mengtao Jia,Xiuli Chen
Tributyltin (TBT) can be used as an antifouling agent with anticorrosive, antiseptic and antifungal properties and is widely used in wood preservation and ship painting. However, it has recently been found that TBT can be harmful to aquatic organisms. In this study, to gain insight into the effects of TBT with respect to the development of the cardiovascular system in zebrafish embryos, zebrafish embryos were exposed to different concentrations of TBT solutions (0.2 μg/L, 1 μg/L, and 2 μg/L) at 2 h post-fertilization (hpf) TBT exposure resulted in decreased hatchability and heart rate, deformed features such as pericardial edema, yolk sac edema, and spinal curvature in zebrafish embryos, and impaired heart development. Expression of cardiac development-related genes ( vmhc , myh6 , nkx2.5 , tbx5a , gata4 , tbx2b , nppa ) is dysregulated. Transgenic zebrafish Tg ( fli1 : EGFP) were used to explore the effects of TBT exposure on vascular development. It was found that TBT exposure could lead to impaired development of intersegmental vessels (ISVs), common cardinal vein (CCV), subintestinal vessels (SIVs) and cerebrovascular. The expression of vascular endothelial growth factor (VEGF) signaling pathway-related genes ( flt1 , flt4 , kdr , vegfa ) was downregulated. Biochemical indices showed that ROS and MDA levels were significantly elevated and that SOD and CAT activities were significantly reduced. The expression of key genes for prostacyclin synthesis ( pla2 , ptgs2a , ptgs2b , ptgis , ptgs1 ) is abnormal. Therefore, it is possible that oxidative stress induced by TBT exposure leads to the blockage of arachidonic acid (AA) production in zebrafish embryos, which affects prostacyclin synthesis and consequently the normal development of the heart and blood vessels in zebrafish embryos.
研究领域:
环境毒理学
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发育生物学
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水生毒理学
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产品关联
DOI
PubMed
高影响因子
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