JOURNAL OF ENVIRONMENTAL MANAGEMENT
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2022
·
IF 8.91
Lu Wang,Yaqun Yu,Guoqiang Liu,Junhe Lu
Tetrabromobisphenol S (TBBPS), an emerging brominated flame retardant , can cause neurotoxic and cytotoxic effects to human physiology . In this study, the degradation of TBBPS in Co 2+ activated peroxymonosulfate (PMS) oxidation process was explored. In particular, brominated by-products formed during the degradation of the TBBPS were examined. It was found that TBBPS could be effectively removed in the Co 2+ /PMS oxidation process. The pseudo-first-order rate constants were 0.13 min −1 at 0.2 mM PMS and 0.5 μM Co 2+ initially. It appeared that TBBPS degradation occurred via and HO attacks, but played a dominant role. The presence of natural organic matter (NOM) greatly inhibited the transformation of the TBBPS, which can be explained by the scavenging of the radical species. β-Scission, debromination, and cross-coupling were identified as the main reaction pathways of TBBPS degradation in the Co 2+ /PMS system. Further oxidation and ring-opening of the intermediates generated brominated by-products including bromoform, monobromoacetic acid, and dibromoacetic acid. The formation of the brominated by-products increased gradually in approximately 48 h. But, the presence of NOM reduced the yields of the brominated -by-products. The findings of this study indicate that organic bromine contaminants can be effectively removed but lead to brominated by-products in the activated PMS oxidation process, which should be taken into consideration when -based oxidation technology is applied.
研究领域:
环境科学
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化学工程
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水处理
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产品关联
DOI
PubMed
高影响因子
CHEMOSPHERE
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2016
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IF 3.698
Weiping Xie,Wei Dong,Deyang Kong,Yuefei Ji,Junhe Lu,Xiaoming Yin
Sulfate radicals (SO 4 − ) generated by activation of peroxymonosulfate (PMS) and persulfate (PS) are highly oxidative and applied to degrade various organic pollutants. This research was designed to investigate formation of halogenated by-products in Co 2+ activated PMS process in the presence of halides and natural organic matter (NOM). It was revealed that no halogenated by-products were detected in the presence of Cl − while 189 μg/L bromoform and 100.7 μg/L dibromoacetic acid (DBAA) were found after 120 h when 2 mg/L NOM, 0.1 mM Br − , 1.0 mM PMS, and 5 μL Co 2+ were present initially. These products are known as disinfection by-products (DBPs) since they are formed in water disinfection processes. Formation of DBPs was even more significant in the absence of Co 2+ . The data indicate that both PMS and SO 4 − can transform Br − to reactive bromine species which react with NOM to form halogenated by-products. Less DBP formation in Co 2+ -PMS systems was due to the further destruction of DBPs by SO 4 − . More DBPs species including chlorinated ones were detected in the presence of both Cl − and Br − . However, more brominated species produced than chlorinate ones generally. The total DBP yield decreased with the increase of Cl − content when total halides kept constant. This is one of the few studies that demonstrate the formation of halogenated DBPs in Co 2+ /PMS reaction systems, which should be taken into consideration in the application of SO 4 − based oxidation technologies .
研究领域:
环境科学
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水处理技术
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF HAZARDOUS MATERIALS
·
2024
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IF 12.2
Qi Tang,Bixi Zhao,Siqi Cao,Shuang Wang,Yue Liu,Yangyang Bai,Jiajun Song,Chuanying Pan,Haiyu Zhao,Xianyong Lan
Disinfection of public drinking water and swimming pools is crucial for preventing waterborne diseases , but it can produce harmful disinfection by-products (DBPs), increasing the risk of various diseases for those frequently exposed to such environments. Bromoacetic acid (BAA) is a ubiquitous DBP, with toxicity studies primarily focused on its in vitro cytotoxicity, and insufficient research on its neurodevelopmental toxicity. Utilizing zebrafish as a model organism, this study comprehensively explored BAA’s toxic effects and uncovered the molecular mechanisms through neurobehavioral analysis, in vivo two-photon imaging, transcriptomic sequencing, pharmacological intervention and molecular biological detection. Results demonstrated BAA induced significant changes on various indicators in the early development of zebrafish. Furthermore, BAA disrupted behavioral patterns in zebrafish larvae across locomotion activity, light-dark stimulation, and vibration stimulation paradigms. Subsequent investigation focused on larvae revealed BAA inhibited neuronal development, activated neuroinflammatory responses, and altered vascular morphology. Transcriptomic analysis revealed BAA-stressed zebrafish exhibited downregulation of visual transduction-related genes and activation of ferroptosis and cellular apoptosis. Neurobehavioral disorders were recovered by inhibiting ferroptosis and apoptosis. This study elucidates the neurodevelopmental toxicity associated with BAA, which is crucial for understanding health risks of DBPs and for the development of more effective detection methods and regulatory strategies.
研究领域:
环境科学
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毒理学
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神经生物学
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DOI
高影响因子
International Journal of Electrochemical Science
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2023
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IF 1.5
Zhiqiao He,Qiong Wang,Junjun Sun,Jianmeng Chen,Shuang Song
To improve the effectiveness of dehalogenation of organic halogen compounds, a series of silver-modified Cu foam electrodes (Ag/Cu foam electrode) was prepared via chemical deposition, using AgNO 3 as the precursor. The crystal structure and morphology of the electrodes were measured by means of X-ray diffraction (XRD) and scanning electron microscopy (SEM). It was found that zero-valence Ag particles dispersed finely on the Cu foam surface and their number increased with Ag loading. Electrocatalytic activity was evaluated by monitoring the debromination of mono-bromoacetic acid (MBAA). The best operational conditions were a silver loading of 2 mg/cm 2 , applied current density of 5.5 mA/cm 2 , and pH 7.0. After five successive cycles, the Ag/Cu electrode remained stable for the electrocatalytic debromination of MBAA. We suggest that the improved electrocatalytic activity of the Ag/Cu electrode is mainly attributable to a strong interaction between MBAA and the Ag particles on the surface of electrode. These findings might be of great significance for improving the electrochemical dehalogenation process.
研究领域:
环境科学
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电化学
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产品关联
DOI
高影响因子
ENVIRONMENTAL TOXICOLOGY
·
2022
·Vol. 37
·期 12
·2910-2923
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IF 4.109
Yuting Wu,Jiwen Liu,Shuhui Liu,Wentao Fan,Chenchen Ding,Zhangshan Gao,Zhihui Tang,Yan Luo,Xizhi Shi,Lei Tan,Suquan Song
Since the outbreak of COVID-19, widespread utilization of disinfectants has led to a tremendous increase in the generation of disinfection byproducts worldwide. Bromoacetic acid (BAA), one of the common disinfection byproducts in the environment, has triggered public concern because of its adverse effects on urinary system in mammals. Nevertheless, the BAA-induced nephrotoxicity and potential mechanism in birds still remains obscure. According to the detected content in the Taihu Lake Basin, the model of BAA exposure in chicken was established at doses of 0, 3, 300, 3000 μg/L for 4 weeks. Our results indicated that BAA exposure caused kidney swelling and structural disarrangement. BAA led to disorder in renal function (CRE, BUN, UA) and increased apoptosis (Bax, Bcl-2, caspase3). BAA suppressed the expression of mitochondrial biogenesis genes (PGC-1α, Nrf1, TFAM) and OXPHOS complex I genes (ND1, ND2, ND3, ND4, ND4L, ND5, ND6). Subsequently, BAA destroyed the expression of Nrf2 antioxidant reaction genes (Nrf2, Keap1, HO-1, NQO1, GCLM, GCLC). Furthermore, renal oxidative damage led to disorder in uric acid metabolism genes (Mrp2, Mrp4, Bcrp, OAT1, OAT2, OAT3) and exacerbated destruction in renal function. Overall, our study provided insights into the potential mechanism of BAA-induced nephrotoxicity, which were important for the clinical monitoring and prevention of BAA.
研究领域:
环境科学
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毒理学
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动物生理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
CHEMICO-BIOLOGICAL INTERACTIONS
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2022
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IF 5.168
Jiwen Liu,Yuting Wu,Shuhui Liu,Zhangshan Gao,Wentao Fan,Chenchen Ding,Zhihui Tang,Shuo Zhang,Xizhi Shi,Lei Tan,Yan Luo,Suquan Song
The bromoacetic acid (BAA) is one of the most teratogenic and neurotoxic disinfection byproducts . Birds take environmental water as their habitat and are inevitably affected by BAA in the environment. However, the neurotoxicity caused by BAA in birds has not been reported and the mechanism remains unclear. In this study, we chose chickens as the avian model to explore the effects of different concentrations of BAA on the brain tissues. Here, we selected the 3 μg/L dose of BAA detected in Tai Lake basin as a reference, and designed 1-, 100-, and 1000-fold of the environmental exposure dose as the experimental doses to explore the neurotoxicity of BAA in birds. Results showed that BAA increased the number of pyknotic nuclear neurons, deformed vascular sheaths, and glial cells in the brain. BAA inhibited the activity of antioxidant enzymes and the expression of antioxidant genes. With the increase of BAA concentration, the oxidative stress-responsive transcription factor NF-κB was activated. Furthermore, BAA remarkably changed the expression of lipid metabolism related genes (i.e., acc , gpat , hmgr , pparα , cpt1 , and ampkα ). Importantly, BAA decreased the mRNA and protein expression levels of autophagy-related genes (i.e., atg5 , ulk1 , beclin1 , and lc3 ). Meantime, BAA increased the mRNA and protein levels of apoptotic and pro-apoptotic genes, such as p53 , bax , cytochrome c , caspase-9 , and caspase-3 . Overall, our study provided new insights into the potential neurotoxic effects of BAA in birds, which was important for the clinical monitoring and prevention of BAA.
研究领域:
毒理学
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神经科学
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环境科学
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产品关联
DOI
PubMed
高影响因子
FREE RADICAL BIOLOGY AND MEDICINE
·
2022
·
IF 8.101
Shuhui Liu,Zhangshan Gao,Wanqiu He,Yuting Wu,Jiwen Liu,Shuo Zhang,Liping Yan,Shengyong Mao,Xizhi Shi,Wentao Fan,Suquan Song
Metabolic dysfunction-associated fatty liver disease (MAFLD) has become the most common chronic liver disorders in the world, and yet has no approved pharmacotherapy due to the etiology is complex. In the last ten years, increasing evidence have identified the environmental pollutants as risk factors for MAFLD. However, the underlying mechanism remains unclear. Our study found that bromoacetic acid (BAA, a typical kind of environmental toxin) increased triglycerides and total cholesterol levels as well as induced obvious hepatic steatosis and inflammation. The lipidomics showed that ferroptosis was implicated in the environmental toxin–linked MAFLD. Besides, the analysis of microbial metabolomics showed significant change of gut microbiome in BAA groups and the content of gut microbiota metabolite (glycochenodeoxycholate, GCDCA) increased sharply. In vitro study, we observed features of ferroptotic cells by transmission electron microscopy after BAA/GCDCA treatment . Besides, we demonstrated that BAA/GCDCA significantly increased iron contents, with upregulating transferrin receptor (TFR) and acyl-CoA synthetase long-chain family 4 (ACSL4) expression levels. By contrast, iron chelator or silencing TFR relieved BAA/GCDCA-induced lipid metabolism disorder and inflammation. What's more, the interaction between TFR and ACSL4 was also identified. Taken together, we found that, in response to environmental toxin , gut microbiota metabolite GCDCA activates TFR-ACSL4-mediated ferroptosis, which triggered subsequent lipid metabolism disorder and inflammation. Moreover, these findings firstly highlighted the functional relevance among ferroptosis, lipid metabolism and gut microbiota metabolite during environmental pollutant exposure, which shed light on the deep mechanism of environmental toxin-related MAFLD, providing potential targets for the prevention of MAFLD.
研究领域:
肝病学
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毒理学
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微生物学
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代谢组学
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脂质组学
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产品关联
DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2024
·
IF 6.2
Yemian Zhou,Yun Liu,Tong Wang,Han Li,Jing He,An Xu
Disinfection by-products (DBPs) generated from water treatment have serious adverse effects on human health and natural ecosystems. However, research on the mutagenicity of DBPs with different chemical structures is still limited. In the present study, we compared the mutagenicity of 8 typical DBPs in human-hamster hybrid (A L ) cells and clarified the mechanisms involved. Our data displayed that the rank order for mutagenicity was as follows: iodoacetamide (IAcAm) > iodoacetonitrile (IAN) > iodoacetic acid (IAA) > bromoacetamide (BAcAm) ≈ bromoacetonitrile (BAN) > bromoacetic acid (BAA), which was confirmed by DNA double strand breaks and oxidative DNA damage. In contrast, bromoform (TBM) and iodoform (TIM) had minimal mutagenicity. The mutation spectrum analysis further revealed that IAN, IAcAm, and IAA could induce multilocus deletions in mammalian cells. Interestingly, nitrogenous DBPs (N-DBPs) and IAA were found to cause varying degrees of iron overload and lipid peroxidation, which was mediated by the activation of the Nrf2/HO-1 signaling pathway. Moreover, the presence of deferoxamine (DFO), an iron ion inhibitor, effectively reduced γ-H2AX and 8-OHdG induced by N-DBPs and IAA. These results indicated that the variations in genotoxicity among DBPs with different structures were associated with their ability to disrupt iron homeostasis. This study provided new insights into the mechanisms underlying the structure-dependent toxicity of DBPs and established a foundation for a more comprehensive understanding and intervention of the health risks associated with DBPs.
研究领域:
环境科学
·
毒理学
·
分子生物学
·
细胞生物学
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产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）