Environmental Technology & Innovation
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2024
·
IF 6.7
Xiao-Huang Chen,Su-Huai Chang,Rui Jiang,Yong-Qiang Tian,Li-Ping Jia,Feng-Jiao Liu,Xu-Guang Huang
Cadmium (Cd), a prevalent pollutant in near-shore seawater ecosystems, poses a significant threat to marine biota. Zinc (Zn) and Cd can have interchangeable physiological effects in marine plankton, and both can influence the synthesis of siliceous walls. Consequently, the concentrations of zinc and silicon may jointly impact the toxicity of Cd. This study endeavors to elucidate the combined effect of silicon (Si) and zinc (Zn) on the growth and physiological responses of the marine diatom species Thalassiosira weissflogii when subjected to Cd-induced stress conditions (190.7 μg L −1 ). Our results reveal statistically improvements ( p <0.05) in biomass production, reductions ( p <0.05) in superoxide dismutase (SOD) activity and extracellular secretion in T. weissflogii when high concentrations of Si (172 µmol L −1 ) and Zn (18.3 nmol L −1 ) were applied simultaneously. Additionally, examination of Cd bioconcentration factors (BCF) derived from Cd uptake kinetics and intracellular Cd content measurements underscores the ability of elevated Si and Zn concentrations to reduce intracellular Cd accumulation ( p <0.05). The ability of Si and Zn to mitigate Cd toxicity was further evidenced by increased cellular biosilica content and maintenance of cell morphology, suggesting a protective role in preserving structural integrity and growth. Our findings underscore the synergistic benefits of Si and Zn in enhancing the resilience of T. weissflogii to Cd stress, providing valuable insights into the potential use of nutrient amendments as a strategy for mitigating heavy metal contamination in marine environments.
研究领域:
海洋生物学
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环境科学
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DOI
高影响因子
PLANT BIOLOGY
·
2020
·Vol. 22
·期 4
·679-690
·
IF 2.167
A. Sami,F. A. Shah,M. Abdullah,X. Zhou,Y. Yan,Z. Zhu,K. Zhou
Melatonin has emerged as an essential molecule in plants, due to its role in defence against metal toxicity. Aluminium (Al) and cadmium (Cd) toxicity inhibit rapeseed seedling growth. In this study, we applied different doses of melatonin (50 and 100 µ m ) to alleviate Al (25 µ m ) and Cd (25 µ m ) stress in rapeseed seedlings. Results show that Al and Cd caused toxicity in rapeseed seedling, as evidenced by a decrease in height, biomass and antioxidant enzyme activity. Melatonin increased the expression of melatonin biosynthesis-related Brassica napus genes for caffeic acid O-methyl transferase ( BnCOMT ) under Al and Cd stress. The genes BnCOMT-1 , BnCOMT-5 and BnCOMT-8 showed up-regulated expression, while BnCOMT-4 and BnCOMT-6 were down-regulated during incubation in water. Melatonin application increased the germination rate, shoot length, root length, fresh and dry weight of seedlings. Melatonin supplementation under Al and Cd stress increased superoxide dismutase, catalase, peroxidase, ascorbate peroxidase, proline, chlorophyll and anthocyanin content, as well as photosynthesis rate. Both Cd and Al treatments significantly increased hydrogen peroxide and malondialdehyde levels in rapeseed seedlings, which were strictly counterbalanced by melatonin. Analysis of Cd and Al in different subcellular compartments showed that melatonin enhanced cell wall and soluble fractions, but reduced the vacuolar and organelle fractions in Al- and Cd-treated seedlings. These results suggest that melatonin-induced improvements in antioxidant potential, biomass, photosynthesis rate and successive Cd and Al sequestration play a pivotal role in plant tolerance to Al and Cd stress. This mechanism may have potential implications in safe food production.
研究领域:
植物学
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环境科学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF HAZARDOUS MATERIALS
·
2013
·
IF 3.925
Ruijuan Qu,Xinghao Wang,Zhengtao Liu,Zhenguang Yan,Zunyao Wang
Cadmium (Cd) compounds are widely distributed toxic environmental and industrial pollutants, and they may bring danger to growth and development of aquatic organisms. The effects of Ca 2+ (as CaCl 2 ), Mg 2+ (as MgSO 4 ), K + (as KCl), pH and complexants (EDTA, the commercial DOM , and three homemade DOMs) on Cd toxicity to Photobacterium phosphoreum were evaluated in standardized 15 min acute toxicity tests . Increases in Ca 2+ concentration resulted in higher EC 50 values, indicating the competition between the two ions for uptake sites at the biotic ligand. Increased waterborne Mg 2+ also reduced Cd toxicity, but to a slightly lesser degree compared with Ca 2+ . The overall decline in EC 50 data with increasing K + in test solutions suggested that Cd toxicity was enhanced at larger K + concentration. The toxicity alleviation by H + was observed over the tested pH range of 5.0–9.0. Additions of complexing agents into the exposure water reduced Cd bioavailability via complexation of Cd 2+ , and complexants from different sources displayed different protective effect. The influence of these toxicity modifying factors was finally incorporated into a model that can predict acute cadmidum toxicity for Photobacterium phosphoreum . After validation with laboratory and natural waters, the developed model could support efforts to improve the ecological relevance of presently applied risk assessment procedures.
研究领域:
环境科学
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毒理学
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DOI
PubMed
高影响因子
ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY
·
2013
·Vol. 32
·期 6
·1420-1425
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IF 2.618
Bing-Lin Zhang,Sheng-Hua Shang,Hai-Tao Zhang,Zahra Jabeen,Guo-Ping Zhang
The effect of sodium chloride (NaCl) on cadmium (Cd) uptake, translocation, and oxidative stress was investigated using 2 tobacco cultivars differing in Cd tolerance. The growth inhibition of the tobacco plants exposed to Cd toxicity was in part alleviated by moderate addition of NaCl in the culture solution. Cadmium concentration of shoots and roots in the 2 cultivars increased with increasing Cd levels in the solution and decreased with the addition of NaCl. The addition of NaCl could alleviate the oxidative stress caused by Cd toxicity, as reflected by reduced production of malondialdehyde and recovered or enhanced activities of antioxidative enzymes catalase and glutathione peroxidase. The results also showed that the enhancement of antioxidative enzyme activity by NaCl for the tobacco plants exposed to Cd stress is related to induced Ca signaling. Environ Toxicol Chem 2013;32:1420–1425. © 2013 SETAC
研究领域:
植物学
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环境科学
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DOI
高影响因子
ENVIRONMENTAL POLLUTION
·
2019
·
IF 5.714
Fang Dong,Pu Wang,Wei Qian,Xing Tang,Xiaoshan Zhu,Zhenyu Wang,Zhonghua Cai,Jiangxin Wang
Ocean acidification (OA) is a global problem to marine ecosystems . Cadmium (Cd) is a typical metal pollutant, which is non-essential but extremely toxic to marine organisms. The combined effects of marine pollution and climate-driven ocean changes should be considered for the effective marine ecosystem management of coastal areas. Previous reports have separately investigated the influences of OA and Cd pollution on marine organisms. However, little is known of the potential combined effects of OA and Cd pollution on marine diatoms. We investigated the sole and combined influences of OA (1500 ppm CO 2 ) and Cd exposure (0.4 and 1.2 mg/L) on the coastal diatom Skeletonema costatum . Our results clearly showed that OA significantly alleviated the toxicity of Cd to S. costatum growth and mitigated the oxidant stress, although the intercellular Cd accumulation still increased. OA partially rescued S. costatum from the inhibition of photosynthesis and pyruvate metabolism caused by Cd exposure. It also upregulated genes involved in gluconeogenesis, glycolysis, the citrate cycle (TCA), Ribonucleic acid (RNA) metabolism, and especially the biosynthesis of non-protein thiol compounds. These changes might contribute to algal growth and Cd resistance. Overall, this study demonstrates that OA can alleviate Cd toxicity to S. costatum and explores the potential underlying mechanisms at both the cellular and molecular levels. These results will ultimately help us understand the impacts of combined stresses of climate change and metal pollution on marine organisms and expand the knowledge of the ecological risks of OA.
研究领域:
海洋生物学
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环境科学
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产品关联
DOI
PubMed
高影响因子
FREE RADICAL BIOLOGY AND MEDICINE
·
2025
·
IF 8.2
Tongwang Luo,Shengzhe Song,Shujie Wang,Sheng Jiang,Bin Zhou,Quanjiang Song,Lingjun Shen,Xiaodu Wang,Houhui Song,Chunyan Shao
Cadmium (Cd), a pervasive environmental toxicant, poses significant threats to human and animal health through multi-organ toxicity. While ferroptosis has been implicated in Cd-induced pathologies, the molecular mechanisms underlying Cd-mediated nephrotoxicity remain poorly understood. This study elucidates the ferroptosis pathway in CdCl 2 -exposed PK-15 cells and murine kidney, characterized by iron overload, lipid peroxidation, and mitochondrial dysfunction, which were ameliorated by ferroptosis inhibitor ferrostatin-1. Transcriptomic analysis revealed substantial upregulation of heme oxygenase-1 (HO-1) following CdCl 2 exposure. Mechanistically, CdCl 2 triggered nuclear translocation of nuclear factor erythroid 2-related factor-2 (NRF2), subsequently activating HO-1 transcription. Over-activated HO-1 catalyzes the decomposition of heme and releases free iron, accompanied with the degradation of ferritin heavy chain 1 (FTH1) induced by CdCl 2 exposure, which leads to intracellular iron overload and excessive lipid peroxides production through Fenton reaction, resulting in ferroptosis ultimately. In vivo validation confirmed NRF2/HO-1-mediated ferroptosis in CdCl 2 -induced murine nephrotoxicity. Both pre-treatment with HO-1 competitive inhibitor Zinc protoporphyrin IX (ZnPP) and knockout of HO-1 gene remarkably alleviated PK-15 cells against ferroptosis induced by CdCl 2 treatment. Our findings demonstrate that Cd exposure initiates NRF2-mediated HO-1 overexpression, driving iron-dependent lipid peroxidation and subsequent ferroptosis. This mechanistic insight provides potential therapeutic targets for mitigating Cd-induced renal damage, advancing our understanding of heavy metal toxicity and its cellular consequences.
研究领域:
毒理学
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细胞生物学
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环境健康科学
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产品关联
DOI
PubMed
高影响因子
SCIENCE OF THE TOTAL ENVIRONMENT
·
2024
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IF 8.2
Zaoli Zhang,Tingting Zhang,Long Lu,Shunjiao Qiu,Zecong Huang,Yuan Wang,Xinyu Chen,Long Li,Yanyan Sun,Rongjun Zhang,Pinghua Chen,Yuanyuan Song,Rensen Zeng
Brassinosteroids (BRs) and jasmonic acid (JA) are known to be involved in regulating plant responses to cadmium (Cd) stress. However, their specific roles and interaction in this process remain unclear. In this study, we discovered that exogenous BR alleviated Cd-mediated growth inhibition of rice seedlings. Enhanced Cd tolerance was also observed in m107 , a BR-overproduction mutant. Phenotypic analysis of genetic materials involved in BR signaling confirmed the positive role of BR in regulating rice response to Cd toxicity. OsDLT, a key component in the BR signaling pathway, was found to be crucial for BR-mediated Cd tolerance. Further analysis demonstrated that activation of the BR pathway reduced the accumulation of Cd and reactive oxygen species (ROS) by modulating the expression of genes associated with Cd transport and ROS scavenging. Interestingly, transcriptome analysis indicated that the JA pathway was enriched in OsDLT-regulated differently expressed genes (DEGs). Gene expression and hormone assays showed that BR promoted the expression of JA pathway genes and JA levels in plants. Moreover, BR-induced tolerance was compromised in the JA signaling-deficient mutant osmyc2 , suggesting that BR-mediated Cd resistance depends on the activation of the JA signaling pathway. Overall, our study revealed the synergistic interaction between BR and JA pathways in rice response to Cd stress, providing insights into the complex hormonal interplay in plant tolerance to heavy metals.
研究领域:
植物学
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环境科学
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分子生物学
✓ 已验证
DOI
PubMed
高影响因子
BIOLOGICAL TRACE ELEMENT RESEARCH
·
2025
·
IF 3.6
Xu Hao,Yang Jingyi,Ye Ruiqi,Cao Mixia,Li Shenghe,Liu Chang,Li Lei
Acute cadmium (Cd) exposure induces hepatic toxicity in murine models, where oxidative stress and subsequent inflammatory responses are recognized as principal contributors to hepatocyte damage. The NLRP3 inflammasome, a pivotal member of the NOD-like receptor family, mediates pyroptotic cell death in diverse hepatic inflammatory pathologies. While murine liver exhibits heightened susceptibility to heavy metal toxicity, the mechanistic basis of Cd-induced hepatocyte injury remains incompletely characterized. This study aims to clarify the cytotoxic effects of Cd on murine hepatocyte line BNL CL.2 and systematically dissect the underlying molecular mechanisms. Via molecular and cellular assays, we evaluated mitochondrial function, reactive oxygen species (ROS) levels, NLRP3 inflammasome activation, and pyroptotic features in BNL CL.2 cells post Cd exposure; intervened with ROS scavengers N-acetylcysteine (NAC) and Mito-TEMPO, and detected transcriptional activity of the antioxidant regulator Nrf2. Experimental data demonstrate that Cd exposure triggers mitochondrial dysfunction coupled with excessive ROS production, concomitant NLRP3 inflammasome activation, and characteristic plasma membrane rupture confirming pyroptosis. Notably, NAC and Mito-TEMPO effectively attenuate these pathological responses, establishing ROS as critical regulators of Cd-induced NLRP3 inflammasome activation; mechanistically, Cd suppresses Nrf2 transcriptional activity and downstream antioxidant gene expression, thereby disrupting redox homeostasis. These findings collectively delineate a pathogenic cascade where Cd impairs mitochondrial integrity and disrupts Nrf2-dependent antioxidant defenses, synergistically driving ROS-mediated NLRP3 inflammasome activation and subsequent hepatocyte pyroptosis. This mechanism provides novel insights into heavy metal hepatotoxicity and identifies potential targets for treating Cd-induced liver injury.
研究领域:
毒理学
·
分子生物学
·
肝病学
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氧化应激
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炎症与免疫
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产品关联
DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2024
·
IF 6.2
Xingyu Chen,Wenqian Sun,Yanting Song,Shangong Wu,Shouqi Xie,Wen Xiong,Chengdong Peng,Yu Peng,Zhengxiang Wang,Sovan Lek,Christer Hogstrand,Mette Sørensen,Lei Pan,Dong Liu
The impact of cadmium (Cd) toxicity on fish liver injury has received much attention in recent years. Currently, autophagy, apoptosis and endoplasmic reticulum stress were reported in Cd exposed fish liver, and if there are other mechanisms (such as ferroptosis) and relevant signaling pathways involved in fish remains unknown. An experiment was conducted to investigate Cd toxicity in Channa argus (Cantor, 1842) exposed to 0, 1.0, and 2.0 mg Cd/L of water for 96 h. Cd disrupted the structure of mitochondria in the liver. Besides, Cd induced ferroptosis by significantly increasing the level of Fe 2+ , ROS, MDA and significantly decreasing the level of Ferritin, GSH, GSH-Px, GPX4, GST and SOD ( p < 0.05 in all cases). In addition, the mRNA expression of ferroptosis related genes, gpx4 and slc7a11 , were significantly downregulated by Cd. Moreover, Cd exposure significantly inhibited the Nrf2/Keap1 signaling pathway, one of the pathways involved in ferroptosis, by upregulating the mRNA levels of keap1a and keap1b , and downregulating the mRNA levels of nrf2 and its target genes ( ho-1 , nqo1 and cat ). Cd exposure also caused extensive accumulation of vacuoles and lipid droplets in liver, as well as an increase in triglyceride content. Cd significantly affected lipid metabolism related enzyme activity and gene expression, which were also regulated by Nrf2/Keap1 signaling pathway. In summary, these results indicate that ferroptosis is a mechanism in waterborne Cd exposed fish liver injury via the Nrf2/Keap1 signaling pathway and the Cd induced hepatic steatosis is also modulated by Nrf2/Keap1 pathway at the whole-body level in fish. These findings provide new insights into the fish liver injury and molecular basis of Cd toxicity.
研究领域:
环境毒理学
·
鱼类生理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
·
2020
·Vol. 27
·期 20
·25278-25286
·
IF 3.056
Wang Jicang,Zhu Huali,Wang Ke,Yang Zijun,Liu Zongping
Cadmium (Cd), a highly toxic heavy metal, adversely affects human and animal health. Quercetin (Que) is a kind of flavonoid that can protect many tissues from the toxic effect of heavy metals. Although many studies have explored the adverse effects of cadmium on rats and other animals, the mechanism of Cd-induced testicular autophagy and the antagonistic effect of Que on cadmium remain unclear. In this study, Sprague–Dawley rats were treated with Cd, Que or Cd, and Que supplements to explore the mechanisms of Que-alleviated testis injury caused by Cd exposure. The rat body weight and relative testicular weight were measured. Morphological changes in testes and indices of oxidative stress were also examined. The expression levels of autophagy-related genes were detected as well. Results showed that Cd decreased the rat body weight and relative testicular weight and induced pathological changes in testes. Conversely, Que alleviated these changes. We also found that Cd increased the malondialdehyde content and decreased the contents of total superoxide dismutase, glutathione peroxidase, catalase, and glutathione. Moreover, the protein expression levels of P62 and LC3-II increased under Cd exposure conditions. Conversely, Que obviously alleviated these toxic activities induced by Cd. Overall, this study showed that Cd accumulated in rat testes, leading to oxidative stress and autophagy. Que can reduce cadmium toxicity by reducing oxidative stress and inhibiting autophagy. The specific mechanism of Que antagonizing Cd toxicity can provide new insights into countering cadmium toxicity.
研究领域:
毒理学
·
药理学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
·
2015
·
IF 4.143
Xinghao Wang,Ruijuan Qu,Jiaoqin Liu,Zhongbo Wei,Liansheng Wang,Shaogui Yang,Qingguo Huang,Zunyao Wang
Experiments were conducted to investigate the effect of four different carbon nanotubes single- and multi-walled carbon nanotubes (SWCNTs and MWCNTs) and hydroxylated and carboxylated multi-walled carbon nanotubes (OH-MWCNTs and COOH-MWCNTs) on Cd toxicity to the aquatic organism Daphnia magna . The acute toxicity results indicated that all CNTs could enhance the toxicity of Cd to D. magna . Furthermore, the filtrate toxicity and adsorption tests showed that the toxicity-increasing effect of SWCNTs and MWCNTs in the overall system was mainly caused by catalysts impurities from the pristine CNTs, whereas the greater adsorption of Cd onto OH-MWCNTs (30.52 mg/g) and COOH-MWCNTs (24.93 mg/g) was the key factor contributing to the enhanced toxicity. This result raised a concern that the metal catalyst impurities, adsorption capacities, and accumulation of waterborne CNTs were responsible for the toxicity of Cd to aquatic organism.
研究领域:
环境科学
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毒理学
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产品关联
DOI
PubMed
高影响因子
Food & Function
·
2016
·Vol. 7
·期 8
·3524-3530
·
IF 2.686
Yuhui Li,Kaiyong Liu,Jie Shen,Yehao Liu
Environmental exposure to pollutants such as heavy metals is responsible for various altered physiological functions that are detrimental to health. Cadmium (Cd) is one of the most representative toxic, non-essential elements that can contaminate food and water. This study evaluated the protective effects of wheat bran, a selected prebiotic with good Cd binding ability, against Cd toxicity in mice. Thirty mice were divided into control and therapeutic groups. The control group was fed a low dietary fiber diet with no Cd for 8 weeks. In the therapeutic group, 100 mg L−1 Cd was administered along with a diet of 10% wheat bran. First, the binding ability of wheat bran for Cd was measured along with the protection of cell growth in vitro by wheat bran. Second, the effectiveness of wheat bran in preventing Cd from entering mice organs was evaluated. Finally, restoration of gut microbiota from alterations caused by Cd was investigated. The results showed that wheat bran could bind most of the Cd ions and restore the growth rate of cells in vitro. The wheat bran treatment group showed that the bran effectively prevented Cd from entering mice organs. In addition, the bacterial community structure was restored because the toxicity of Cd to gut microbiota was eliminated by the wheat bran. Our results suggest that wheat bran is more effective against chronic Cd toxicity than traditional treatments because of its special physiological functions, and it can be considered as a new dietary, therapeutic strategy against Cd toxicity.
研究领域:
环境科学
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营养学
·
微生物学
·
毒理学
✓ 已验证
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）