乐果对秀丽隐杆线虫生活史特征的影响

采用一种半流体培养基"挂滴法"对线虫进行培养和生命表实验,研究了低剂量暴露下乐果对秀丽隐杆线虫生活史特征的影响。在半致死浓度1/10 LC50、1/100 LC50、1/1000 LC50暴露剂量下(分别为7、0.7、0.07 mmol·L-1)染毒4 h。结果表明,0.7和7 mmol·L-1暴露组线虫的总繁殖率(TFR)分别为260.60、203.80,明显低于对照组(299.23,P0.05);净增殖率(R0)分别为240.29、147.67,明显低于对照组(298.67,P0.05);内禀增长率(rm)分别为1.342 d-1、1.233 d-1,明显低于对照组(1.387 d-1,P0.05);而0.07 mmol·L-1暴露组线虫的总繁殖率为293.84,净增殖率为286.60,与对照组比差异都没有统计学意义(P0.05)。在上述浓度范围,线虫的总繁殖率(TFR)、净增殖率(R0)和内禀增长率(rm)都随乐果浓度的升高而降低,并存在剂量效应关系。研究同时发现0.07 mmol·L-1暴露组线虫的内禀增长率为1.405 d-1,明显高于对照组(P0.05)。研究结论认为一定剂量的乐果使线虫的繁殖力降低;而低剂量暴露则对内禀增长率具有毒物兴奋效应。本文选择的3个指标TFR、R0、rm对低剂量下乐果暴露的响应敏感。     

Toxicity of nanoparticulate and bulk ZnO, Al2O3 and TiO2 to the nematode Caenorhabditis elegans

Limited information is available on the environmental behavior and associated potential risk of manufactured oxide nanoparticles (NPs). In this research, toxicity of nanoparticulate and bulk ZnO, Al₂O₃ and TiO₂ were examined to the nematode Caenorhabditis elegans with Escherichia coli as a food source. Parallel experiments with dissolved metal ions from NPs were also conducted. The 24-h median lethal concentration (LC₅₀) and sublethal endpoints were assessed. Both NPs and their bulk counterparts were toxic, inhibiting growth and especially the reproductive capability of the nematode. The 24-h LC₅₀ for ZnO NPs (2.3 mg L⁻¹) and bulk ZnO was not significantly different, but significantly different between Al₂O₃ NPs (82 mg L⁻¹) and bulk Al₂O₃ (153 mg L⁻¹), and between TiO₂ NPs (80 mg L⁻¹) and bulk TiO₂ (136 mg L⁻¹). Oxide solubility influenced the toxicity of ZnO and Al₂O₃ NPs, but nanoparticle-dependent toxicity was indeed observed for the investigated NPs.     

重金属对秀丽隐杆线虫繁殖的影响

为了探究重金属单独及联合暴露对秀丽隐杆线虫(Caenorhabditis elegans)繁殖的影响及其作用机制,采用96孔板液相暴露试验,以环境相关浓度(0.1~50.0 μg/L)的Cd、Hg、Pb暴露同步化处理秀丽隐杆线虫,24 h后统计其怀卵数及阴门畸形率,以及连续记录72 h内子一代秀丽隐杆线虫的个体数,最后利用2×2析因设计方差分析阐明重金属的两两联合作用模式. 结果表明:与对照组相比,Cd、Hg、Pb单独及联合暴露对秀丽隐杆线虫的繁殖具有显著抑制作用,ρ(Cd)为50.0 μg/L、ρ(Hg)为10.0 μg/L、ρ(Pb)为50.0 μg/L暴露组秀丽隐杆线虫子一代数量分别降低了43.5%、33.8%、51.0%;Cd-Hg暴露组〔当ρ(Cd)、ρ(Hg)分别为50.0、10.0 μg/L时〕、Hg-Pb暴露组〔当ρ(Hg)、ρ(Pb)分别为10.0、50.0 μg/L时〕、Cd-Pb暴露组〔当ρ(Cd)、ρ(Pb)分别为50.0、50.0 μg/L时〕秀丽隐杆线虫子一代个体数分别降低了44.7%、61.0%、53.3%. 进一步研究发现,Cd、Hg、Pb单独及联合暴露会引起秀丽隐杆线虫子宫内受精卵数量降低以及产卵器阴门结构畸形率升高. 2×2析因设计方差分析结果发现,Cd、Hg、Pb两两联合暴露对秀丽隐杆线虫的繁殖表现为没有交互作用或者交互方式为拮抗. 研究显示,秀丽隐杆线虫子宫内怀卵数的降低是其子一代数量显著减少的主要原因,而阴门结构的损伤可能使产卵行为受损,从而进一步加剧重金属对秀丽隐杆线虫繁殖的抑制作用.      

Carbamazepine, carbamazepine epoxide and dihydroxycarbamazepine sorption to soil and occurrence in a wastewater reuse site in Tunisia

Although a number of manufactured nanoparticles are applied for the medical and clinical purposes, the understanding of interaction between nanomaterials and biological systems are still insufficient. Using nematode Caenorhabditis elegans model organism, we here investigated the in vivo toxicity or safety of hydroxylated fullerene nanoparticles known to detoxify anti-cancer drug-induced oxidative damages in mammals. The survival ratio of C. elegans rapidly decreased by the uptake of nanoparticles from their L4 larval stage with resulting in shortened lifespan (20 d). Both reproduction rate and body size of C. elegans were also reduced after exposure to 100 μg mL⁻¹ of fullerol. We found ectopic cell corpses caused by apoptotic cell death in the adult worms grown with fullerol nanoparticles. By the mutation of core pro-apoptotic regulator genes, ced-3 and ced-4, these nanoparticle-induced cell death were significantly suppressed, and the viability of animals consequently increased despite of nanoparticle uptake. The apoptosis-mediated toxicity of nanoparticles particularly led to the disorder of digestion system in the animals containing a large number of undigested foods in their intestine. These results demonstrated that the water-soluble fullerol nanoparticles widely used in medicinal applications have a potential for inducing apoptotic cell death in multicellular organisms despite of their antioxidative detoxifying property.     

基于土壤模式生物的纳米材料毒理研究进展

随着纳米科技与工业的高速发展,大量的纳米材料被广泛应用并最终汇聚到土壤环境中,对土壤生态和人体健康造成潜在影响。由于土壤生物具有多样性,选择具有代表性、敏感性并便于获取的土壤模式生物作为实验受体进行纳米材料的生物安全评估及环境毒理效应研究尤为重要。较为系统地回顾和总结了几种典型土壤模式生物的特点,为纳米材料毒理研究中受试生物的选择提供参考,在此基础上整理了大量基于典型土壤模式生物的纳米材料毒性研究资料,归纳了不同层次的研究方法,分析探索了纳米材料毒性机理,并展望了未来的研究重点。     

生物炭中持久性自由基对秀丽隐杆线虫的毒性

为了评价生物炭的使用对生态系统,尤其是对土壤无脊椎动物的毒性影响,使用模式生物秀丽隐杆线虫（Caenorhabditis elegans,C.elegans）来评估生物炭的环境风险.观察了生物炭原样、生物炭颗粒物和生物炭浸提液对线虫神经行为学评价指标（身体摆动频率、相对运动长度、排泄间隔时间、碰触反应率和化学感知行为指数）的影响;并结合生物炭的理化性质、非金属元素组成和重金属元素含量以及环境持久性自由基（EPFRs）的强度,评估生物炭对线虫的生物毒性.结果显示,EPFRs信号强的生物炭和颗粒物对秀丽隐杆线虫有一定的毒物兴奋效应,EPFRs信号微弱的浸提液无显著性影响.因此,生物炭中的EPFRs对秀丽隐杆线虫有潜在的神经毒性作用.     

Using the nematode Caenorhabditis elegans as a model animal for assessing the toxicity induced by microcystin-LR

Among more than 75 variants of microcystin(MC),microcystin-LR(MC-LR) is one of the most common toxins.In this study,the feasibility of using Caenorhabditis elegans to evaluate MC-LR toxicity was studied.C.elegans was treated with MC-LR at different concentrations ranging from 0.1 to 80 μg/L.The results showed that MC-LR could reduce lifespan,delay development,lengthen generation time,decrease brood size,suppress locomotion behavior,and decreases hsp-16-2-gfp expression.The endpoints of generation time,brood...     

Induction of chemotaxis to sodium chloride and diacetyl and thermotaxis defects by microcystin-LR exposure in nematode Caenorhabditis elegans

Apart from the liver disruption, embryotoxicity and genotoxicity, microcystin (MC)-LR also could cause neurotoxicity. Nematode Caenorhabditis elegans was explored as a model to study the neurotoxicity. In the present study, we provided evidence to indicate the neurotoxicity on chemotaxis to NaCl and diacetyl, and thermotaxis from MC-LR exposure to C. elegans. As a result, higher concentrations of MC-LR caused significantly severe defects of chemotaxis to NaC1 and diacetyl, and thermotaxis. The neurotoxicity on chemotaxis to NaCl and diacetyl, and thennotaxis from MC-LR exposure might be largely mediated by the damage on the corresponding sensory neurons (ASE, AWA, and AFD) and interneuron AIY. The expression levels of che-1 and odr-7 were significantly decreased (P<0.01) in animals exposed to MC-LR at concentrations lower than 10 μg/L, whereas the expression levels of ttx-1 and ttx-3 could be significantly (P<0.01) lowered in animals even exposed to 1 μg/L of MC-LR. Moreover, both the chemotaxis to NaCl and diacetyl and the thermotaxis were more significantly reduced m MC-LR exposed mutants of che-1(p674), odr-7(ky4), ttx-1(p767), and ttx-3(ks5) than those in exposed wild-type N2 animals at the same concentrations.     

Adverse effects of metal exposure on chemotaxis towards water-soluble attractants regulated mainly by ASE sensory neuron in nematode Caenorhabditis elegans

Chemotaxis to water-soluble attractants is mainly controlled by ASE sensory neuron whose specification is regulated by che-1 in Caenorhabditis elegans. Our data suggested that exposure to high concentrations of metals, such as Pb, Cu, Ag, and Cr, would result in severe defects of chemotaxis to water-soluble attractants of NaCl, cAMP, and biotin. Moreover, the morphology of ASE neuron structures as observed by relative fluorescent intensities and relative size of fluorescent puncta of cell bodies, relative lengths of sensory endings in ASE neurons, and the expression patterns of che-1 were obviously altered in metal exposed animals when they meanwhile exhibited obvious chemotaxis defects to water-soluble attractants. In addition, the dendrite morphology could be noticeably changed in animals exposed to 150 mol/L of Pb, Cu, and Ag. Furthermore, we observed significant decreases of chemotaxis to water-soluble attractants in Pb exposed che-1 mutant at concentrations more than 2.5 mol/L, and in Cu, Ag, and Cr exposed che-1 mutant at concentrations more than 50 mol/L. Therefore, impairment of the ASE neuron structures and functions may largely contribute to the appearance of chemotaxis defects to water-soluble attractants in metal exposed nematodes.     

The toxicological paradigms of aluminum and the etiology of Alzheimer's disease in the nematode Caenorhabditis elegans

This study examined behavioral and enzymatic changes of C. elegans from its exposure to aluminum, and the resulting relationship with Alzheimer's disease. After chronic and acute exposure to aluminum, the results indicated that it alters the cholinergic status and behavior parameters of the nematode, suggesting a relationship between exposure to aluminum and the etiology of AD.