5种卤代乙酰胺类消毒副产物对小鼠淋巴瘤细胞Tk基因致突变性研究

卤代乙酰胺类(HAc Am)消毒副产物(DBPs)是饮用水中新兴含氮类DBPs之一。为探究HAc Ams的致突变性,选择小鼠淋巴瘤细胞作为受试细胞,分别考察了一氯代乙酰胺、二氯代乙酰胺、三氯代乙酰胺、一碘代乙酰胺、二碘代乙酰胺(DIAc Ams)共5种HAc Ams对小鼠淋巴瘤细胞Tk基因突变的影响。结果表明,在0.05~20μmol·L~(-1)暴露浓度下,5种HacAms类DBPs对小鼠淋巴瘤细胞呈现出一定的细胞毒性,随着暴露浓度的升高,细胞毒性增强。暴露4 h后,5种HacAms中只有DIAc-Ams呈现出显著的致突变性(暴露剂量高于5μmol·L~(-1)),且以小集落为主。上述研究结果为研究HacAms对哺乳动物细胞的致突变作用提供了基础数据。     

妇女乳腺癌医院出院率与在含持久性有机污染物场地邮政区居住之间的关系

持久性有机污染物(persistent organic polutants,简称POPs)大多具有毒性,有的甚至致癌,但目前对POPs引起的健康风险仍知之甚少。本研究的假设是在含POPs场地邮政区居住妇女的乳腺癌风险增大。从纽约州计划与研究合作系统(SPARCS)等数据库中收集乳腺癌患者的信息及居住地危险废弃物暴露、经济收入和城市化等数据。以邮政区编码表征居住地,采用负二项回归方法,对纽约州30岁以上妇女乳腺癌医院出院率进行了模型分析,参数包括种族、年龄、污染暴露、经济收入和城市化率。结果显示,不同参数之间(如暴露与种族、暴露与收入、暴露与城市化)存在交互作用。对部分子群而言,与居住在不含危险废弃物场地邮政区的妇女相比,居住在含POPs场地邮政区的妇女乳腺癌出院率显著升高(率比(rate ratio,RR)1.10~1.34,P0.05)。这种关系在非裔妇女中强于白种妇女、在城市化高的地区强于农村地区。调整了混杂因素后,某些妇女人群乳腺癌出院率升高与在含POPs场地邮政区居住有显著的关系。     

Role of the necrosis factor-κB pathway in dibutyl phthalate mediated effects on human glioma cells

Abstract

The human glioma cell line U251 was incubated for 12?h and 24?h in medium containing dibutyl phthalate at concentrations of 25?µmol/L and 100?µmol/L. Decreased cell viability and increased oxidative stress show the cytotoxicity of dibutyl phthalate. Nuclear factor-κB and nuclear factor-κB pathway-related proteins were altered, which could be attenuated by vitamin E at 20?µmol/L. Thus, dibutyl phthalate induces cytotoxicity through activation of nuclear factor-κB and vitamin E exerts neuroprotection against dibutyl phthalate-mediated cytotoxicity in vitro.     

Assessment of DNA damage and cytotoxicity of palmatine on human skin epithelial carcinoma cells

The present investigation was carried out to examine the cytotoxic and genotoxic effects of a Tinospora cordifolia crude methanolic extract (palmatine) on human skin epithelial carcinoma cells (A431). T. cordifolia is one of the indispensable medicinal plants used in Ayurvedic medicine for treatment of various diseases and recommended for improving the immune system. Cytotoxicity and genotoxicity evaluation was carried out using A431 cells treated with different concentrations of palmatine. The duration of the treatment was 24 and 48 hr. A cellular proliferative capacity test showed that palmatine produced cytotoxicity in concentration- and time-dependent manner. Further, palmatine induced significant intracellular reactive oxygen species generation and elevated lipid peroxidation, as well as activities of catalase and superoxide dismutase. DNA fragmentation analysis using the comet assay showed that palmatine induced genotoxicity in a concentration- and time-dependent manner. Evidence indicates palmatine is capable of induction of oxidative stress resulting in cell death and genomic instability.     

Enzymatic and cellular level effects of chromium∗

Exposure of Cr to four hepatic enzymes activities of tilapia, viz. acid‐ and alkaline phosphatases, catalase and glucose‐6‐phosphatase, was contrary to the results obtained for Cd and Ni. This is the only heavy metal investigated thus far that dramatically augmented glucose‐6‐phosphatase by approximately 83% at a concentration of 12 mg L^‐1 in vivo in lieu of the fact of an initial inhibition of approximately 45 % at a lower concentration of Cr; 6 mg L^‐1. In the case of acid phosphatase and catalase activities progressive increment was observed up to 50 and 217% respectively at a concentration of 12 mg L^‐1 Cr. On the other hand, in contrast to all the investigated enzymes interestingly alkaline phosphatase was inhibited continuously at all concentrations up to 46% at 12 mgL^‐1 Cr. In vitro experiments were contrary to the above mentioned results, whereby all hepatic enzymes were inhibited with major inhibition observed for acid phosphatase of approximately 60% from 5 mgL^‐1 Cr onwards in the system.

At cellular level, Cr exposure at a lethal dose of 12 mgL^‐1 demonstrated similar effects to that of Cd. In general, the glycogen and fat reserves were depleted while lysosomal activity is increased. As compared to the effects of Cd, the mitochondria did not indicate any prominent reflection in the formation of intramitochondrial bodies. Further, similar to Cd, the cell membrane as well as nucleus were not affected.     

活性氧介导砷诱导的蚕豆保卫细胞死亡

采用蚕豆(Vicia fabaL.)表皮条生物法,研究砷的细胞毒性作用机制。结果发现,一定浓度的NaAsO2可使气孔保卫细胞活性降低,部分细胞死亡,细胞死亡率呈浓度依赖性增高;砷处理组保卫细胞内活性氧(reactive oxygen species,ROS)水平升高。抗氧化剂抗坏血酸和过氧化氢酶及Ca2+特异性螯合剂EGTA、Ca2+通道抑制剂LaC13与NaAsO2共同作用时,砷诱发的细胞死亡被显著抑制;MAPK激酶抑制剂PD98059亦能有效阻止NaAsO2诱发的细胞死亡。研究结果表明,砷胁迫引起的胞内ROS合成增加可能通过Ca2+信号途径介导了保卫细胞的死亡过程,MAPK途径参与了砷诱导的细胞死亡。     

Comparison of basal cytotoxicity of seven carbamates in CHO-K1 cells

The cytotoxic effects of seven carbamate pesticides, aldicarb, aldicarb sulfone, aldicarb sulfoxide, benfuracarb, pirimicarb, propoxur and thiobencarb, were compared in Chinese hamster ovary (CHO-K1) cell line of Circetulus griseus. The endpoints evaluated were lysosomal function by neutral red assay and mitochondrial integrity by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT assay). The carbamates tested were evaluated in both serum-free medium and in serum-containing medium. Results demonstrate that CHO-K1 lysosomes appeared more susceptible to propoxur, aldicarb and its metabolites than mitochondria. Aldicarb was the most toxic carbamate pesticide tested on CHO-K1 cells and aldicarb sulfoxide the least. The presence of foetal calf serum (FCS) diminished significantly the cytotoxicity of tested carbamates.     

水体中铊对泥鳅外周血红细胞的遗传毒性的时效性

铊(T1)是剧毒的重金属元素,会对生态环境和人体健康造成威胁.目前各国铊的环境安全标准存在差异.本文利用泥鳅红细胞微核技术,研究泥鳅Misgurnus anguillicaudatus红细胞微核率和核异常率与铊污染时间的关系,为该技术在铊毒理研究中的可行性和铊环境安全标准提供依据.结果表明:水体铊质量浓度为0.5μg·L~(-1)下,随处理时间的延长,泥鳅红细胞微核率、核异常率显著增加,并与时间呈显著的正相关,其中微核率、核异常率分别在处理24 h和48 h时达到最大值;随后两指标逐步下降,与时间呈显著的负相关.在此铊质量浓度和处理时间内,核异常率与微核率均显著高于空白无铊对照处理,表明水体铊质量浓度0.5 μg·L~(-1)对泥鳅血红细胞具有遗传毒性.     

量子点对Cu2+诱导L02细胞毒性的影响及机理研究

量子点(QDs)和Cu~(2+)可能共存于肝脏,对肝细胞产生联合毒性,威胁人体健康。本研究以人胚肝细胞(L02)为研究对象,考察了低/无毒的QDs(3.6%的细胞致死率)对Cu~(2+)诱导L02细胞毒性的影响及相关机理,为其可能的健康和环境风险提供参考。结果显示,QDs的加入使得Cu~(2+)的细胞毒性有了很大的提高,细胞存活率最高下降了26.0%,两者表现为协同作用;另外QDs存在使得Cu~(2+)细胞蓄积量增大,伴随着Cu~(2+)天然解毒蛋白CTR1和ATP7A等表达水平的升高,从侧面印证了Cu~(2+)的蓄积量增加对细胞的影响;同时,QDs的存在使得细胞乳酸脱氢酶(lactate dehyfrogenase,LDH)泄露相对于Cu~(2+)单独处理组提高,暗示QDs可能破坏了细胞膜,导致Cu~(2+)在细胞内蓄积量增加,从而使细胞毒性增加,两者的联合毒性表现为协同作用。     

利用休止细胞法选择性脱除燃料油中有机硫

红球菌(Rhodococcus sp .)FS-1菌株能通过专一性断裂C—S键的途径脱除二苯并噻吩 (DBT)中的有机硫作为自身生长需要的硫源 ,从而降低油品中的硫含量 .本文利用该菌的休止细胞对DBT和柴油的脱硫活力进行了研究 .结果表明 ,该菌株对DBT及柴油中的有机硫均有良好的选择性脱除作用 .DBT浓度为0.5～1.0mmol/L、油水比例为 1:5时 ,脱硫效果最佳 .采用二次脱硫法可使柴油脱硫率达85%以上 ,证明FS-1能有效脱除柴油中的有机硫 .烃质组分的气相色谱分析表明 ,FS-1作用前后的柴油烃类组分基本没有改变 ,说明该菌的脱硫作用是特异性针对硫原子的 ,不会破坏柴油的有效成分 .