水飞蓟的毒理学安全性评价

目的：对水飞蓟进行毒理学安全性评价,为其食用安全性提供科学依据。方法：采用大鼠急性毒性实验、Ames实验,小鼠骨髓细胞微核实验、精子畸形实验和大鼠30d喂养实验等安全性评价实验,评估水飞蓟的食用安全性。结果：水飞蓟对雌、雄大鼠的急性经口最大耐受量（MTD）均大于18.0g/kg·BW。Ames实验、小鼠骨髓微核验和精子畸形实验结果均未见该样品有致突变作用,大鼠30d喂养实验各项指标也均未见明显毒性反应。结论：水飞蓟急性毒性分级属无毒级、无遗传毒性,在该实验研究剂量和条件下,水飞蓟未见明显毒副作用。     

细颗粒物(PM2.5)与植被关系的研究综述

细颗粒物即PM,2.5,粒径小,沉降困难,危害严重,植被在一定程度上有助于减轻颗粒物污染.本文从阐述PM2.5的沉降机理出发,分析PM2.5与植被之间的相互作用.植被的阻滞吸收作用对大气颗粒物移除存在积极影响,而过多的空气颗粒物滞留对植物生长起到一定的负面作用,但以植被对大气颗粒物的移除为主导作用.以此为基础,从林分尺度-环境特性、单木尺度-树种特性和叶片尺度-颗粒物种类和分布特性这3个角度出发,结合外界影响因素(气象学要素、空气动力学要素、大气颗粒浓度水平、植物物候变化)、气室实验以及滞留颗粒物特征等阐述植被林冠、枝干及叶片等对移除PM2.5的影响.最后,文章指出今后的研究应当向定量化方向发展,注重不同树种移除PM2.5能力的对比分析及系统研究,并针对研究区域确定防治大气PM2.5污染的优势树种.     

园林植物吸附细颗粒物(PM_(2.5))效应研究进展

园林植物具有显著消减空气颗粒物(PM)污染的作用,能有效地改善城市环境质量。但迄今为止,国内外的大量研究都集中在园林植物对总悬浮颗粒物(TSP)或者粗颗粒物(PM10)的阻滞效应上,植物吸附空气细颗粒物(PM2.5)的研究尚处于探索阶段。本文概述了植物叶片吸附空气PM的方式,叶片PM2.5化学物质的转移过程以及植物吸附PM2.5的周期性,探讨了植物叶片对空气不同粒径颗粒物的吸附特征,园林植物吸附空气PM2.5的能力与机制,并从植物吸附PM2.5的测定方法、园林植物吸附PM2.5能力的测定和评价、高吸附PM2.5能力的园林植物筛选、园林植物吸附PM2.5的机制与影响因素等方面提出了园林植物吸附PM2.5的研究重点与趋势,以期为深化植物吸附PM2.5的机制研究及高吸附PM2.5能力的园林植物筛选提供依据。     

北京市湿地削减大气细颗粒物PM_(2.5)功能

基于野外观测与遥感反演相结合的方法,在点位和区域尺度上研究北京城区湿地在削减大气细颗粒物PM2.5中的作用。结果表明,北京城区湿地能够显著削减周边大气环境中的细颗粒物浓度,其中翠湖湿地附近的PM2.5浓度显著低于周边裸地(P0.05),可削减空气中17%的PM2.5,降低幅度最高可达50%。而且,湖库湿地在削减PM2.5浓度方面作用更加显著,优于河流湿地(P0.05)。北京市PM2.5浓度的空间分布格局表现出西北东南、郊区城区的空间分布规律。因此,在未来的湿地建设中应合理选择湿地类型,更多地考虑紧凑型湿地如湖库湿地的建设,科学配置湿地和植物资源,使湿地更加有效地发挥其增湿、促使局地流场发生变化的作用,最终改善局地微气象条件,削减大气细颗粒物,缓解城市雾霾天气。研究结果为北京市湿地保护管理、规划和布局以及及时制定控制PM2.5的政策和措施提供了科学依据。     

低分子质量魔芋甘露寡糖的长期毒性与遗传毒性研究

魔芋甘露寡糖是一种具有肠道菌群调节作用的新型食品添加剂．本研究首次通过酶解与有机溶剂沉淀法制备了低分子质量的甘露寡糖(聚合度2～7),并对这类寡糖进行了长期毒性与遗传毒性评价．在长期毒性试验中,以大鼠为实验对象,分低、中、高(2.25,5.25,7.50 g/kg)药物剂量组和阴性对照组,连续灌胃给药90天．一般状况观察、生化指标、血液学指标、病理学等与对照组比较均无显著性差异,而大体解剖观察发现,部分大鼠的肝脏与肾脏形态发生变化,但这些变化均在正常范围内,且其他各项指标差异均无统计学意义．此外,一系列实验包括小鼠骨髓微核实验、Ames试验、小鼠精子畸变试验均未发现低分子质量甘露寡糖有明显的遗传毒性．试验结果提示,本研究方法获得的低分子质量甘露寡糖在本实验条件下未发现长期毒性与遗传毒性．     

细颗粒物对呼吸系统疾病的影响

大城市阴霾天气的频频出现,引起社会对其罪魁祸首——细颗粒物(即PM2.5)的广泛关注。PM2.5对健康的影响成为人们普遍担忧的问题。本文综述了PM2.5与呼吸系统疾病关系的流行病学研究进展。结果显示,短期暴露于较高浓度的PM2.5与哮喘急诊就诊率、慢性阻塞性肺病(COPD)患者急性加重住院率、肺炎急诊住院率的上升及COPD日死亡风险的增加均有关;长期暴露于较高浓度的PM2.5与肺癌及肺炎死亡风险增加、肺腺癌和哮喘发病风险增加有关。上述研究结果大部分来自西方发达国家,提示了我国有效控制PM2.5浓度及开展更多关于PM2.5流行病学研究的必要性和紧迫性。     

低分子质量魔芋甘露寡糖的长期毒性与遗传毒性研究（英文）

魔芋甘露寡糖是一种具有肠道菌群调节作用的新型食品添加剂.本研究首次通过酶解与有机溶剂沉淀法制备了低分子质量的甘露寡糖(聚合度2~7),并对这类寡糖进行了长期毒性与遗传毒性评价.在长期毒性试验中,以大鼠为实验对象,分低、中、高(2.25,5.25,7.50 g/kg)药物剂量组和阴性对照组,连续灌胃给药90天.一般状况观察、生化指标、血液学指标、病理学等与对照组比较均无显著性差异,而大体解剖观察发现,部分大鼠的肝脏与肾脏形态发生变化,但这些变化均在正常范围内,且其他各项指标差异均无统计学意义.此外,一系列实验包括小鼠骨髓微核实验、Ames试验、小鼠精子畸变试验均未发现低分子质量甘露寡糖有明显的遗传毒性.试验结果提示,本研究方法获得的低分子质量甘露寡糖在本实验条件下未发现长期毒性与遗传毒性.     

姜黄素通过抑制凋亡信号调节激酶1减弱PM2.5短期暴露致大鼠子宫损伤

细颗粒物(PM2.5)是空气动力学直径≤2.5 μm的颗粒物,能诱发多种疾病.已有大量的流行病学调查证实,PM2.5能够损伤生殖系统,但其致病机制不明确,相关的研究也非常有限.为研究PM2.5短期暴露对大鼠子宫的损伤,以及姜黄素(curcumin,CRC)对其保护作用,本研究将50只雌性SD大鼠随机分为生理盐水对照组、...     

大气颗粒物对健康的影响

<正>近年来研究发现,大气颗粒物严重影响人体健康,PM2.5每年造成80万人死亡,排在所有致死因素的第13位[1].大气颗粒物是悬浮于空气中颗粒的总称,按照其空气动力学粒径分为总悬浮颗粒物(TSP空气动力学直径小于100μm,下同)、可吸入颗粒物(PM10)、细颗粒物(PM2.5)和超细颗粒物(PM0.1)[2].不     

北京大兴南海子公园PM2.5 和PM10 质量浓度变化特征

对北京南海子公园PM2.5 和PM10 的浓度水平进行了研究, 并讨论了PM2.5 和PM10 的时间变化特征及其受气象因素的影响, 分析了南海子公园空气质量浓度差异。结果表明: 南海子公园PM2.5 和PM10 平均质量浓度分别为(110.22±19.19) μg·m3和(125.58±3.62) μg·m3, 南海子公园大气颗粒物主要是以细粒子为主, PM2.5 超标46.96 %, PM10 未超标; 南海子公园PM2.5 和PM10质量浓度的日变化以夜间低, 白天高为主, 呈现明显的双峰型, 南海子公园的PM2.5和PM10质量浓度变化幅度较大; 从不同月份来看, 南海子公园PM2.5 质量浓度6 月最大、8 月最低; 温度、风和降水与PM2.5 和PM10 质量浓度呈负相关关系, 湿度与PM2.5 和PM10 质量浓度呈正相关关系, 大风和降雨能有效的清除颗粒物, 特别是细颗粒物。     

嗜酸乳杆菌LA-G80的毒理学研究

目的对嗜酸乳杆菌的毒性进行研究。方法采用大、小鼠急性毒性试验、Ames试验、小鼠骨髓细胞微核试验、小鼠精子畸形试验和大鼠30 d喂养等对嗜酸乳杆菌进行安全性试验研究。结果急性经口毒性试验表明,大、小鼠灌胃给予嗜酸乳杆菌,最大耐受剂量雌雄两性别均大于20.0 g/kg体重,Ames试验、微核试验和精子畸形试验结果均为阴性。大鼠30 d喂养试验结果表明各项指标均未见明显毒性反应。结论在本次实验条件下,嗜酸乳杆菌未见遗传毒性。由此可初步判定,使用嗜酸乳杆菌是安全可靠的。     

The Salmonella mutagenicity of industrial, surface and ground water samples of Aligarh region of India

The genotoxicity of three water bodies, viz. industrial waste water of Aligarh city, ground water pumped out from the industrial area of Aligarh, and river water of Yamuna, downstream of Agra, was carried out by means of Ames plate incorporation test and the Ames fluctuation test. All the test samples were significantly mutagenic in both the testing systems. The ground water and river water samples were subjected to XAD concentration prior to the mutagenicity/genotoxicity testing, while the industrial waste water was used directly. Whereas TA98, TA102 and TA104 strains have been found to be maximally sensitive in the Ames plate incorporation assay conducted for various water samples, TA98 and TA100 strains were the most responsive strains in the Ames fluctuation test. The apparent disparity in the sensitivity patterns of various Ames strains by plate incorporation and fluctuation assays could be attributed to a large extent to the different conventional ways of interpretation of the data in these systems.     

Genotoxicity of silver nanoparticles evaluated using the Ames test and in vitro micronucleus assay

Silver nanoparticles (AgNPs) have antimicrobial properties, which have contributed to their widespread use in consumer products. A current issue regarding nanomaterials is the extent to which existing genotoxicity assays are useful for evaluating the risks associated with their use. In this study, the genotoxicity of 5 nm AgNPs was assessed using two standard genotoxicity assays, the Salmonella reverse mutation assay (Ames test) and the in vitro micronucleus assay. Using the preincubation version of the Ames assay, Salmonella strains TA102, TA100, TA1537, TA98, and TA1535 were treated with 0.15-76.8 μg/plate of the AgNPs. Toxicity limited the doses that could be assayed to 2.4-38.4 μg/plate; no increases in mutant frequency over the vehicle control were found for the concentrations that could be assayed. Human lymphoblastoid TK6 cells were treated with 10-30 μg/ml AgNPs, and additional cells were treated with water and 0.73 gy X-rays as vehicle and positive controls. Micronucleus frequency was increased by the AgNP treatment in a dose-dependent manner. At a concentration of 30 μg/ml (with 45.4% relative population doubling), AgNPs induced a significant, 3.17-fold increase with a net increase of 1.60% in micronucleus frequency over the vehicle control, a weak positive response by our criteria. These results demonstrate that the 5 nm AgNP are genotoxic in TK6 cells. Also, the data suggest that the in vitro micronucleus assay may be more appropriate than the Ames test for evaluating the genotoxicity of the AgNPs.     

Organic extracts of urban air pollution particulate matter (PM2.5)-induced genotoxicity and oxidative stress in human lung bronchial epithelial cells (BEAS-2B cells)

Traffic is a major source of particulate matter (PM), and ultrafine particulates and traffic intensity probably contribute significantly to PM-related health effects. As a strong relationship between air pollution and motor vehicle-originated pollutants has been shown to exist, air pollution genotoxicity studies of urban cities are steadily increasing. In Korea, the death rate caused by lung cancer is the most rapidly increased cancer death rate in the past 10 years. In this study, genotoxicity of PM2.5 (<2.5μm in aerodynamic diameter particles) collected from the traffic area in Suwon City, Korea, was studied using cultured human lung bronchial epithelial cells (BEAS-2B) as a model system for the potential inhalation health effects. Organic extract of PM2.5 (CE) generated significant DNA breakage and micronucleus formation in a dose-dependent manner (1μg/cm(3)-50μg/cm(3)). In the acid-base-neutral fractionation of PM2.5, neutral samples including the aliphatic (F3), aromatic (F4) and slightly polar (F5) fractions generated significant DNA breakage and micronucleus formation. These genotoxic effects were significantly blocked by scavenging agents [superoxide dismutase (SOD), sodium selenite (SS), mannitol (M), catalase (CAT)]. In addition, in the modified Comet assay using endonucleases (FPG and ENDOIII), CE and its fractions (F3, F4, and F5) increased DNA breakage compared with control groups, indicating that CE and fractions of PM2.5 induced oxidative DNA damage. These results clearly suggest that PM2.5 collected in the Suwon traffic area has genotoxic effects and that reactive oxygen species may play a distinct role in these effects. In addition, aliphatic/chlorinated hydrocarbons, PAH/alkylderivatives, and nitro-PAH/ketones/quinones may be important causative agents of the genotoxic effects.     

一株白腐菌的食用安全性初步评价

本研究选取了一株白腐菌模式菌株进行了小鼠急性毒性试验、小鼠骨髓嗜多染红细胞微核试验以及小鼠精子畸形试验,以分析该白腐菌的食用安全性,为进一步应用白腐菌开发功能性食品提供数据支持。结果显示,小鼠经灌胃白腐菌,其LD50为6.76 g/kg(以白腐菌菌丝干重计)。微核试验和精子畸形试验结果均为阴性(P0.05)。试验结果表明,本次实验条件下,白腐菌对小鼠表现出一定的急性毒性,但未见遗传毒性,由此推断,在一定剂量范围内使用白腐菌作为食用材料是相对安全的,安全的剂量范围需要进一步扩大浓度梯度来确定。     

In vitro genotoxicity testing strategy for nanomaterials and the adaptation of current OECD guidelines

There is a pressing requirement to define a hazard identification and risk management strategy for nanomaterials due to the rapid growth in the nanotechnology industry and their promise of life-style revolutions through the development of wide-ranging nano-containing consumer products. Consequently, a battery of well defined and appropriate in vitro assays to assess a number of genotoxicity endpoints is required to minimise extensive and costly in vivo testing. However, the validity of the established protocols in current OECD recognised genotoxicity assays for nanomaterials is currently being questioned. In this report, we therefore consider the in vitro OECD genotoxicity test battery including the Ames, micronucleus and HPRT forward mutation assays, and their potential role in the safety assessment of nanomaterial induced DNA damage in vitro.     

In vitro short-term test evaluation of catecholestrogens genotoxicity

Estrogens are indicated as being the most important etiological factors for the development and progression of breast cancer. The implication of estrogen in breast cancer has been associated mostly with the estrogen receptors that mediate cell proliferation. Evidence also exists to support the hypothesis of a direct role of estrogens as tumor initiators. However, the role of estrogen genotoxicity in breast cancer is still questionable.

In this study the genotoxic activity of catecholestrogens and 16-hydroxy estrone has been investigated by performing Salmonella strain TA98 and TA100 Ames tests, sister chromatide exchange assays (SCE) and micronucleus assays on human peripheral lymphocytes (CBMN and ARA/CBMN). We found a lack of positive results with micronucleus assays, except for 2-hydroxy estradiol (2-OHE₂), which shows a peculiar “bell shaped” trend of micronucleus number versus concentrations. SCE assay suggests weak genotoxic activity of all tested catechol metabolites, except 4-hydroxy estrone (4-OHE₁), which also showed negative results by ARA/CBMN.

In this open debate, our results support the hypothesis of a weak genotoxicity, not correlated with the carcinogenetic potential of estrogens.     

A core in vitro genotoxicity battery comprising the Ames test plus the in vitro micronucleus test is sufficient to detect rodent carcinogens and in vivo genotoxins

In vitro genotoxicity testing needs to include tests in both bacterial and mammalian cells, and be able to detect gene mutations, chromosomal damage and aneuploidy. This may be achieved by a combination of the Ames test (detects gene mutations) and the in vitro micronucleus test (MNvit), since the latter detects both chromosomal aberrations and aneuploidy. In this paper we therefore present an analysis of an existing database of rodent carcinogens and a new database of in vivo genotoxins in terms of the in vitro genotoxicity tests needed to detect their in vivo activity. Published in vitro data from at least one test system (most were from the Ames test) were available for 557 carcinogens and 405 in vivo genotoxins. Because there are fewer publications on the MNvit than for other mammalian cell tests, and because the concordance between the MNvit and the in vitro chromosomal aberration (CAvit) test is so high for clastogenic activity, positive results in the CAvit test were taken as indicative of a positive result in the MNvit where there were no, or only inadequate data for the latter. Also, because Hprt and Tk loci both detect gene-mutation activity, a positive Hprt test was taken as indicative of a mouse-lymphoma Tk assay (MLA)-positive, where there were no data for the latter. Almost all of the 962 rodent carcinogens and in vivo genotoxins were detected by an in vitro battery comprising Ames+MNvit. An additional 11 carcinogens and six in vivo genotoxins would apparently be detected by the MLA, but many of these had not been tested in the MNvit or CAvit tests. Only four chemicals emerge as potentially being more readily detected in MLA than in Ames+MNvit--benzyl acetate, toluene, morphine and thiabendazole--and none of these are convincing cases to argue for the inclusion of the MLA in addition to Ames+MNvit. Thus, there is no convincing evidence that any genotoxic rodent carcinogens or in vivo genotoxins would remain undetected in an in vitro test battery consisting of Ames+MNvit.     

In vitro genotoxicity of danthron and its potential mechanism

To ascertain the in vitro genotoxicity of danthron and its potential mechanism of action, we performed an Ames test, a cytokinesis-block micronucleus assay and a comet assay in Balb/c 3T3 cells. The Ames test revealed that danthron was mutagenic only toward Salmonella typhimurium strain TA102 in the presence of an exogenous metabolic activation system (S9 mix). Danthron (25, 50 and 100μg/ml) increased the frequencies of micronuclear cells with or without S9 mix, and the comet length, tail length and Olive tail moment in comet assays without S9 mix in a dose-dependent manner. These results demonstrated the in vitro genotoxicity of danthron and that 3T3 cells are capable of activating danthron. When NADP was replaced by NAD in the S9 mix, danthron remained mutagenic toward strain TA102. The addition of dicoumarol, a DT-diaphorase inhibitor, decreased the number of danthron-induced histidine revertants by 35-39%, indicating that DT-diaphorase is involved in the metabolic activation of danthron in the presence of NADH as an electron donor. In 3T3 cells, increases in reactive oxygen species (ROS) formation and 8-hydroxydeoxyguanosine levels as well as a reduction in GSH levels were induced by danthron in a dose-dependent manner, indicating that oxidative stress may be a major contributing pathway in the genotoxicity of danthron.     

Comparative chemical analysis,mutagenicity, and genotoxicity of Petroleum refinery wastewater and its contaminated river using prokaryotic and eukaryotic assays

Concern on the toxicity of final wastewater generated by the petroleum refining industry has increased in recent years due to the potential health threats associated with their release into the waterways. This study determined the mutagenic and genotoxic potential of petroleum refinery wastewater and a receiving river using the Ames fluctuation test on Salmonella typhimurium strains TA100 and TA98, SOS chromotest on Escherichia coli PQ37, and piscine peripheral micronucleus (MN) assay. Analyses of the physicochemical parameters, heavy metal, and organic contents of the samples were also performed. Ames test result showed that the two tested samples were mutagenic with TA100 strain as the more responsive strain for both the refinery wastewater and the river sample in terms of the calculated mutagenic index. A similar result was obtained in the SOS chromotest; however, the E. coli PQ37 system recorded a slightly higher sensitivity for detecting genotoxins than the Salmonella assay in the two samples. MN data showed induction of a concentration-dependent significant (p < 0.05) increase in the frequency of MN by both samples when compared with the negative control. Generally, the refinery wastewater induced the highest mutagenicity and genotoxicity compared to the river sample in the three assays used. Haemoglobin, platelets, red blood cells, mean corpuscular volume, total white blood cells, heterophils, haematocrit, and eosinophils reduced significantly with increased lymphocytes, basophils, mean corpuscular haemoglobin, and mean corpuscular haemoglobin concentration in fishes exposed to both samples. Total petroleum hydrocarbon, benzene, toluene, phenol index, polycyclic aromatic hydrocarbons, cadmium, mercury, nickel, lead, and vanadium contents analysed in the samples were believed to be responsible for the observed genotoxicity and mutagenicity. The findings of this study revealed that petroleum refinery wastewater is a potential mutagenic and genotoxic risk to the environment.