Effect of nutrient conditions on the toxicity of naphthalene to Chlorella pyrenoidosa

The toxicity of naphthalene to a freshwater microalga, Chlorella pyrenoidosa, and the subsequent recovery of algae from the damage were investigated under two nutrient conditions, either enriched with nitrogen (N) and phosphorus (P), or starved of N and P. Results showed that C. pyrenoidosa was more sensitive to naphthalene under N,P-enriched condition, and the inhibitory rate generally increased at first and then decreased gradually with the evaporation of naphthalene under both nutrient conditions. Enriched N, P reduced the inhibitory rate at initial naphthalene concentration of 5 and 10 mg/L, but enhanced it at 100 mg/L, at which more severe ultrastructure damages were found than those under N,P-starved condition. Observed damages included partly or totally disappearance of nucleolus, nuclear, and plasma membranes. According to the chlorophyll content and cell density measurements, C. pyrenoidosa could recover from naphthalene damage with initial concentrations 6 50 mg/L in 7 days under both nutrient conditions, while they could not recover if the initial concentration of naphthalene was at 100 mg/L. Under the N,P-starved condition, the inability of C. pyrenoidosa to recover from the naphthalene damage was consistent with the results of high inhibitory rate, low value of specific growth rate (SGR, 0.05 day??1), and the severe destruction of cell structure. However, under the N,P-enriched conditions, the observed lower inhibitory rate, higher value of SGR (0.55 day??1), and the intact cell structure of most cells suggested that algae could potentially recover from the naphthalene damage.     

大型溞母溞暴露于氨氮所产子代对氨氮毒性的耐受性

采用大型溞(Daphnia magna)作为受试生物,在测定了氨氮对大型溞的急慢性毒性效应的基础上,进一步研究了在慢性毒性试验中暴露于氨氮环境下的母溞所产子代对氨氮的毒性响应.急性毒性试验结果表明,氨氮对大型溞的24 h和48 h的LC50分别为165.97和69.54 mg/L.21 d慢性试验结果表明:大型溞的生长指标——脱皮数是对氨氮最为敏感的毒性参数;其慢性毒性下限值(LCL)和慢性毒性上限值(UCL)分别为1.88和3.75 mg/L;据此计算出的慢性毒性值(CHV)为2.66 mg/L,急慢性比(ACR)为26.14.在慢性试验中,暴露于毒物的母体所产的子代幼溞,与对照组相比,其48 h LC50都有所增大(增幅为13.7%～56.2%),说明对毒物的适应性有所增强.     

生活垃圾焚烧飞灰制陶瓷砖表征

为了探索生活垃圾焚烧飞灰资源化利用途径,在对飞灰化学组成及矿物成分分析的基础上,利用飞灰、黄陶土、耐火砂及长石研制陶瓷砖,最佳配比方案为:飞灰20%,黄陶土60%,长石10%,耐火砂10%,分析了最佳配比制品的吸水率、抗压强度、微观结构及水平振荡浸出毒性。结果表明:飞灰属SiO2-Al2O3-金属氧化物体系,主要矿物成分是钙硅酸盐及铝硅酸盐等,可用于制陶瓷砖;最佳配比制品达MU15强度等级,满足抗风化的要求;随煅烧温度的升高,制品结构不断密实化,960℃烧成的制品显示出完全烧结的特点,960~1 000℃烧成的制品中出现明显的晶化、玻璃化过程。最佳配比制品重金属浸出毒性完全达标,重金属的浸出率与坯体相比大大降低。     

受污染地表水的生物毒性效应分析

针对以非常规水源补水的受污染地表水的生态安全问题,文章以北京地区受污染河水为试验用水,利用多组生物效应试验(发光菌、大型蚤和仔鱼)进行急性生物毒性检测,并与污水厂二级出水和再生水厂出水水质进行比较.结果表明:受污染地表水在浓缩倍数达50倍时,发光细菌相对抑制率达到50％以上,大型蚤和仔鱼的急性毒性试验死亡率均达到100...     

藻毒素复合污染对鱼体的免疫毒性研究

针对水体富营养化问题,通过单一暴露和联合暴露方式研究两种MCs四种暴露剂量（0．1,1,10,100μg／L）下对鱼体的免疫毒效应。结果发现,不同剂量MCLR和MCRR单一暴露都能使鲫鱼淋巴细胞发生死亡,呈现明显的剂量效应和时间效应关系。且MCLR对鱼体的毒性相对McRR要更显著;MCLR和McRR复合暴露对鱼体淋巴细胞的毒性效应表现为协同作用,且随着毒素浓度的增加,其毒性效应差异显著性也随之升高,故而鱼体的免疫系统造成重大的影响,因此应当加强控制藻毒素在水体中的复合污染。     

DELtatox便携式毒性测试仪在Q—TOX和B—TOX两种模式下应用与探讨

随着经济社会的发展,突发性水质污染事故日趋增多。因此能够快速、准确测定水质状况是环境应急监测的一项重要工作。在一起水厂取水口有人投药打鱼事故中,采用DELtatox便携式毒性测试仪在Q—TOX和B—TOX两种模式下快速检测事发地水质,结果表明快速、高效的检测为此次污染事故的成功处置提供了技术支持,为以后类似突发污染事故的应急监测提供了参考。     

PU合成革废水治理分析

生产聚氨酯（PU）合成革的废水中含有高浓度有机物,其中N,N-二甲基甲酰胺（DMF）毒性大,难生物降解.文章阐述了合成革的生产工艺,分析该过程中DMF废水形成阶段、处理现状及其处理方法.结合各种方法的优缺点,展望了DMF废水的处理研究方向.     

废旧线路板中主要有价金属的生物反应器浸出研究

为探讨可供实际生物浸出应用的反应器规模废旧线路板中有价金属浸出特性和工艺条件,通过设计序批式生物浸出反应器,采用分离到的氧化亚铁硫杆菌Z1作为菌种资源,在考察废旧线路板中有价金属的浸出特性的基础上,确定了反应器运行的最佳工艺条件.结果表明,反应器运行的最佳工艺条件为曝气量1L/min、停留时间30h、搅拌速率300r/min以及粉末投加量12g/L.在此条件下,经过101h可以浸出90.24%的铜.同时,经197h的浸出,可以溶出93.06%的镁、92.00%的锌、85.59%的铝和64.51%的镍.因此,生物浸出反应器能有效回收废旧线路板中的有价金属,为该技术的实际应用提供了实验证据.     

Evaluating the effectiveness of marine actinobacterial extract and its mediated titanium dioxide nanoparticles in the degradation of azo dyes

Aim of the present study was to synthesize titanium dioxide nanoparticles （YiO2 NPs） from marine actinobacteria and to develop an eco-friendly azo-dye degradation method. A total of five actinobacterial isolates were isolated from Chennai marine sediments, Tamilnadu, India and analyzed for the synthesis of TiO2 NPs using titanium hydroxide. Among these, the isolate PSV 3 showed positive results for the synthesis of TiO2 NPs, which was confirmed by UV analysis. Further characterization of the synthesized TiO2 NPs was done using XRD, AFM and FI＇-IR analysis. Actinobacterial crude extract and synthesized TiO2 NPs was found efficient in degrading azo dye such as Acid Red 79 （AR-79） and Acid Red 80 （AR-80）. Degradation percentage was found to be 81% for AR-79, 83% for AR-80 using actinobacterial crude extract and 84% for AR-79, 85% for AR-80 using TiO2 NPs. Immobilized actinobacterial ceils showed 88% for AR-79 and 81% for AR- 80, dye degrading capacity. Degraded components were characterized by FT-IR and GC-MS analysis. The phytotoxicity test with 500 μg/mL of untreated dye showed remarkable phenotypic as well as cellular damage to Tagetes erecta plant. Comparatively no such damage was observed on plants by degraded dye components. In biotoxicity assay, treated dyes showed less toxic effect as compared to the untreated dyes.     

Primary neuronal-astrocytic co-culture platform for neurotoxicity assessment of di-(2-ethylhexyl) phthalate

Plastics such as polyvinyl chlorides （PVC） are widely used in many indoor constructed environments; however, their unbound chemicals, such as di-（2-ethylhexyl） phthalates （DEHP）, can leach into the surrounding environment. This study focused on DEHP＇s effect on the central nervous system by determining the precise DEHP content in mice brain tissue after exposure to the chemical, to evaluate the specific exposure range. Primary neuronal-astrocyte co-culture systems were used as in vitro models for chemical hazard identification of DEHP. Oxidative stress was hypothesized as a probable mechanism involved, and therefore the total reactive oxygen species （ROS） concentration was determined as a biomarker of oxidative stress. In addition, NeuriteTracer, a neurite tracing plugin with ImageJ, was used to develop an assay for neurotoxicity to provide quantitative measurements of neurological parameters, such as neuronal number, neuron count and neurite length, all of which could indicate neurotoxic effects. The results showed that with 1 nmol/L DEHP exposure, there was a significant increase in ROS concentrations, indicating that the neuronal-astrocyte cultures were injured due to exposure to DEHP. In response, astrocyte proliferation （gliosis） was initiated, serving as a mechanism to maintain a homeostatic environment for neurons and protect neurons from toxic chemicals. There is a need to assess the cumulative effects of DEHP in animals to evaluate the possible uotake and effects on the human neuronal system from exoosure to DEHP in the indoor environment.