大气悬浮颗粒物不同有机组分的致突变性研究

本文根据城市功能区选择４个点采样，颗粒物提取物分成五个组分，分别测定致突变性，结果发现：ＰＡＨ组份，有机酸组分和极性化合物组份有较强的致突变性，冬季颗粒物致突变性比夏季颗粒物致突变性强；主要引起ＴＡ９８菌株的移码型突变，加入活化系统可不同程度地增加提取物致突变性。表明上海市大气污染已是一个严重的，亟待解决的问题。     

西安市大气悬浮颗粒物污染现状及其有机提取物致突变性研究

目的：了解西安市采暖期和非采暖期的大气总悬浮颗粒物（TSP）浓度及其有机提取物的致突变性。方法：根据西安市城市功能分区，用网格式布点法，选择了4个大气质量监测点（工业区，混合区，交通繁忙区和对照区），于采暖期和非采暖期，共采集大气悬浮颗粒物样品96份，分别采用增重法和Ames试验，对样品中大气TSP浓度和有机提取物的致突变性进行测定。结果：西安市大气TSP采暖期为0.5865mg/m^3，非采暖期为0．3535mg/m^3，采暖期TSP浓度显著高于非采暖期（P＜0．05），且两期TSP浓度均显著高于其各自对照区（P＜0．05）。各采样点TSP的有机提取物致突变性检测结果显示各功能区均可检出致突变阳性样品，同一季节各监测点致突变性检出率无显著性差异（P＞0．05），但采暖期致突变阳性检出率显著高于非采暖期（P＜0．05）。结论：西安市大气TSP水平呈现明显的季节性并以采暖期最高；燃煤可能是造成西安市大气TSP致突变性增强的主要原因之一。     

苯并a芘对人胎气管上皮细胞生物大分子作用的探讨

苯并ａ芘（ＢａＰ）是烧煤和吸烟过程中最常见的化学污染物，为了解其在人类肺癌发生中的作用，用人胎肝肺组织和气管支气管上皮细胞（ＨＦＢＥ）研究了ＢａＰ的代谢、几种主要代谢物的致微核（ＭＮ）作用、对程序外ＤＮＡ合成（ＵＤＳ）的影响和对Ｈ－ｒａｓ癌基因的致突变作用。结果发现人胎肝肺组织的微粒体酶都有代谢ＢａＰ的能力，初级代谢产物中有三种二氢二醇苯并ａ芘的衍生物，两种羟基苯并ａ芘代谢物和一种醌基苯并ａ芘。用于试验的ＢａＰ的五种主要代谢物均可诱发ＨＦＢＥ的ＵＤＳ，其中以ａｎｔｉ－ＢＰＤＥ和７．８－ｄｉｏｌＢａＰ最为明显；有三种代谢物可致微核率升高，也是ａｎｔｉ－ＢＰＤＥ的作用最强。用ＰＣＲ－ＲＦＬＰ法发现ａｎｔｉ－ＢＰＤＥ处理后，ＨＦＢＥ中Ｈ－ｒａｓ癌基因的第１２位密码子发生了点突变。本研究对Ｂａｐ的致肺癌作用的可能机制从分子水平上提供了进一步的资料。     

艾条燃烧烟雾抽提物的致突变性研究

艾条燃烧烟雾抽提物的致突变性研究金复生，顾正华，朱瑞娟（上医大金山医院，职业医学研究室，中医科上海２００５４０）我们对针灸科医师常用的艾条燃烧后的烟雾抽提物进行致突变性研究。艾条燃烧经封闭系统抽泸，抽泸物洗脱后配成各种受试浓度。用Ａｍｅｓ法和ＳＣＥ方...     

化工废水非挥发性有机污染物致突变性的研究

本研究采用大孔树脂富集四种化工废水中非挥发性有机物，通过Ａｍｅｓ，ＳＯＳ、鱼类血细胞微核率三种生物试验方法检验其致突变性；结果表明，四种化工废水均含有致突变物，其中以炼油、印染两种废水的致突变性最强。     

化工废水蜚 挥发性有机污染物致突变性的研究

本研究采用大孔树脂富集四种化工放心水中非挥发性有机物，通过Ａｍｅｓ，ＳＯＳ、鱼类血细胞微核率三种生物试验方法检验其致突变性；结果表明，四种化工废水均含有致突变物，其中以炼油、印染两种废水的致突变性最强。     

卵巢恶性肿瘤的筛选诊断

对７９例卵巢良恶性肿瘤患者和５４例正常对照组的血清免疫球蛋白Ｅ（ＩｇＥ）、乳酸脱氢酶（ＬＤＨ）和碱性磷酸酶（ＡＫＰ）指标进行检测。结果：（１）卵巢恶性肿瘤三项指标均高于良性组和对照组；（２）ＩｇＥ和ＬＤＨ对卵巢恶性肿瘤诊断性能差异无显著性，而明显高于ＡＫＰ；（３）ＩｇＥ和ＬＤＨ联合检测，可有于卵巢恶性肿瘤的筛选诊断，二者均阳性，应高度怀疑卵巢恶性肿瘤。     

育发剂致突变性2种试验方法的比较

背景与目的:探讨检测育发剂致突变性的适宜的方法.材料与方法:运用Ames试验、小鼠淋巴瘤细胞试验(MLA)对3种育发剂的致突变性进行研究.结果:28种育发剂中有85.72%的样品对组氨酸缺陷型鼠伤寒沙门氏菌均有程度不同的抑菌或杀菌作用,选取的3种育发剂对组氨酸缺陷型鼠伤寒沙门氏菌均有较强的抑菌杀菌作用,在试验浓度下均未呈现致突变性;MLA试验结果显示,1号样品和3号样品育发剂在测试浓度下未呈现致突变性;2号样品育发剂随浓度增大,L5178Y细胞TK位点的突变频率有升高的趋势,其中8 μl/ml、40 μl/ml和200 μl/ml剂量组的突变率,与对照组相比差异有统计学意义(P＜0.05).结论:小鼠淋巴瘤细胞试验(MLA)可做为毒性较大育发剂的遗传毒性筛检的补充试验.     

NNK诱发人支气管上皮细胞恶性转化及氧化损伤机理研究

本文研究ＮＮＫ诱发人支气管上皮细胞（ＢＥＰ２Ｄ）恶性转化及其氧化损伤机理。结果表明,５００μｇ／ｍｌ的ＮＮＫ作用后的第５代细胞具有抗清生长能力,第１５代细胞具有锚着独立生长特征,第２５代细胞具有裸鼠体内成瘤性,提示ＮＮＫ诱发ＢＥＰ２Ｄ细胞发生了恶性转化。ＮＮＫ作用后,ＢＥＰ２Ｄ细胞产生的过氧化氢（Ｈ２Ｏ２）、超阴离子（Ｏ２）和羟自由基（．ＯＨ）,以及８－羟基脱氧鸟嘌呤（ＯＨ８ｄＧ）含量均显著增高,     

鲁奇低温煤焦油的致突变性及致突变性组份的鉴定

本文将致突变性研究与化学分级和化学组份鉴定相结合,研究讨论了鲁奇低温煤焦油样品的致突变性及致突变性分布,讨论了样品的致突变性来源,并对显著致突变性级分的化学组份进行了分析鉴定。 煤焦油样品经酸碱提取分离为酸性、碱性和中性组分,中性组分和碱性组分再经硅胶柱制备色谱分别分为N_1—N_6六个级分和B_1-B_3三个级分。Ames试验表明,对样品     

亚硝化煤尘提取物的致突变性与煤样中挥发分含量的关系初探

本文报道测定采自山西省五煤矿烟煤样品(5种)挥发分含量结果,并将其亚硝化提取物的致穷变性进行比较,结果显示:烟煤A、B、C、E和F挥发分含量(％)分别为16.27、13.14、16.65、26.87和24.56,其中以烟煤E挥发分含量最高。5种煤样亚硝化提取物致突变性检测结果表明:煤样E和F的亚硝化提取物经Ames试验和SOS显色试验,其结果均呈现致突变性,且E煤样致突变性强于F煤样。本研究结果提示:烟煤样品中挥发分含量与其亚硝化提取物的致突变性有一定相关关系。挥发分含量较高的煤样,其亚硝化提取物的致突变性相应也较强。     

沿淮河某市自来水有机提取物对小鼠的诱变性研究

目的:探讨某市自来水有机提取物对小鼠的诱变性.方法:采集淮河水源水、自来水厂滤池出水、氯化消毒自来水及大型贮水箱水各200 L.经吸附,提取有机物后予小鼠灌胃染毒,检测胸骨骨髓嗜多染红细胞微核率和精子畸形率,并作U检验.结果:淮河水源水及氯化消毒的自来水均有一定的致突变性.毒性大小依次为氯化消毒的自来水>贮水箱水>水源水>滤池出水.结论:淮河水源水已受到有机诱变物的污染,混凝沉淀具有去除有机物、降低源水诱变性作用,而氯化消毒使水质的诱变性增高.     

THE MUTAGENICITY STUDY OF ELSHOLTZIA CILIATA

本文采用Ａｍｅｓ试验，小鼠微核试验及小鼠睾丸染色体畸变试验，对香薷进行了致突变性研究。结果均呈阴性。     

氯硝西潘的致突变性研究

本文采用小鼠骨髓嗜多染红细胞微核试验,小鼠染色体畸变试验及小鼠精子畸形试验,研究了抗癫痫药物氯硝西潘的致突变性,通过对三种不同剂量的试验,发现试验组与阴性对照组均胆非常显著差异（Ｐ〈０．０１）,结果表明氯硝西潘有明显的致突变作用。     

DNA polymerase zeta accounts for the reduced cytotoxicity and enhanced mutagenicity of cisplatin in human colon carcinoma cells that have lost DNA mismatch repair.

The mutagenicity of cis-diamminedichloroplatinum(II) (DDP; cisplatin) and the rate at which resistance develops with repeated exposure to DDP are dependent on mutagenic translesional replication across DDP DNA adducts, mediated in part by DNA polymerase zeta, and on the integrity of the DNA mismatch repair (MMR) system. The aim of this study was to determine whether disabling Pol zeta by suppressing expression of its hREV3 subunit in human cancer cells can reduce the mutagenicity of DDP and whether loss of MMR facilitates mutagenic Pol zeta-dependent translesional bypass. The HCT116+ch3 (MMR(+)/REV3(+)) and HCT116 (MMR(-)/REV3(+)) human colon carcinoma cell lines were engineered to suppress hREV3 mRNA by stable expression of a short hairpin interfering RNA targeted to hREV3. The effect of knocking down REV3 expression was to completely offset the DDP resistance mediated by loss of MMR. Knockdown of REV3 also reduced the mutagenicity of DDP and eliminated the enhanced mutagenicity of DDP observed in the MMR(-)/REV3(+) cells. Similar results were obtained when the ability of the cells to express luciferase from a platinated plasmid was measured. We conclude that Pol zeta plays a central role in the mutagenic bypass of DDP adducts and that the DDP resistance, enhanced mutagenicity, and the increased capacity of MMR(-)/REV3(+) cells to express a gene burdened by DDP adducts are all dependent on the Pol zeta pathway.     

某饮用水氯化消毒前后不同阶段水样的致突变性研究

目的与方法:本文采用Ames 试验、小鼠骨髓嗜多染红细胞微核试验、鱼外周血有核红细胞微核试验,对基本饮用水的水源水、出厂水、末稍水、水泥水箱水、开水经XAD - 2 大孔树脂吸附、丙酮洗脱的浓缩物进行致突变性研究。结果与结论:结果发现:各水样的浓缩物均具有致突变作用。致突变活性的大小依次为出厂水、开水、末稍水、水泥水箱水、水源水。     

Mutagenicity of five arylamines after metabolic activation with isolated dog and human hepatocytes

The mutagenicity of benzidine (BZ) N-acetylbenzidine (MABZ), N,N'-diacetylbenzidine (DABZ), 4-aminobiphenyl (4-AB) and 2-aminoanthracene (2-AA) towards Salmonella typhimurium strain TA1538 was measured in the presence of isolated hepatocytes from dog and man. The influence of paraoxon, an inhibitor of the deacetylation reaction, on the mutagenicity of these compounds was also investigated. Obvious interspecies differences in the mutagenic activation of benzidine and its acetylated-derivatives were seen. However, with liver cell preparations from both species it was found that MABZ and DABZ were more mutagenic than BZ itself. 4-AB appeared to be weakly mutagenic in the presence of human hepatocytes but non-mutagenic with dog hepatocytes. 2-AA was highly mutagenic in both species. When human hepatocytes were used as the metabolic factor, the mutagenicity of all arylamines decreased in the presence of paraoxon. With dog hepatocytes, however, the mutagenicity of all arylamines except DABZ was enhanced in the presence of paraoxon.     

Increased mutagenicity of chloroethylnitrosoureas in the presence of a rat liver S9 microsome mixture

The mechanism for an enhanced effect of Aroclor 1254-induced Sprague-Dawley rat liver 9,000 x g supernatant (S9) microsome preparation on the mutagenicity of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), 1-(2-chloroethyl)-3-cyclohexyl-N-nitrosourea (CCNU), and 2-[3-(2-chloroethyl)-3-nitrosoureido]-2-deoxy-D-glucopyranose (chlorozotocin) for Salmonella typhimurium strain TA1535 was studied. Although all three compounds were direct-acting mutagens, rat liver S9 increased the mutagenic response to BCNU, CCNU, and chlorozotocin. The enhanced mutagenic effect was independent of NADPH. Heat-denatured S9 enhanced the mutagenicity of BCNU and CCNU, but not that of chlorozotocin. Mutagenic enhancement, however, was less than that observed with untreated S9. The substitution of extractable S9 lipid and bovine serum albumin for S9 in the reaction mixture resulted in an enhanced mutagenicity of CCNU with little or no effect on BCNU or chlorozotocin mutagenicity. These results suggest that the enhanced mutagenicity of CCNU, and possibly that of BCNU, in the presence of S9 was due in part to nonspecific factors that are present in the S9 preparation.     

Mutagenicity of the Drinking Water Supply in Bangkok

Seventeen samples of tap water in Bangkok and 2 neighboring provinces were collected in winter and summer, ‍concentrated and tested for mutagenic activity using the Ames Salmonella mutagenesis assay. Preliminary results ‍demonstrated that concentrated tap water exhibited clear mutagenicity towards S. typhimurium TA100 and YG1029, ‍but not towards TA98 and YG1024, in the absence of S9 mix, and the addition of S9 mix markedly decreased the ‍mutagenicity to both tester strains. Amberlite XAD-2 resin, but not blue rayon, was able to adsorb mutagens from ‍water at pH 2. Our data clearly demonstrated that all tap water samples prepared by chlorination of Chao Phraya River water ‍were mutagenic to strain TA100 without S9 mix, inducing 3,351 ± 741 and 2,216 ± 770 revertants/l, in winter and ‍summer, respectively. On the other hand, however, tap water samples prepared from ground water were not mutagenic. ‍Furthermore, it was found that boiling for only 5 min and filtration through home purifying system containing ‍activated charcoal and mixed resin units were very effective to abolish the mutagenicity of water. Storage of water ‍also significantly decreased the mutagenicity, however, it took 2-3 weeks to totally abolish it. Additionally, we also ‍found 1 out of 6 brands of commercially available bottled drinking water to be mutagenic, with about 26 % of the ‍average mutagenicity of tap water. ‍The results in the present study clearly demonstrated that chlorinated tap water in Bangkok and neighboring ‍provinces contain direct-acting mutagens causing capable of causing base-pair substitution. Boiling and filtration of ‍tap water through home purifying systems may be the most effective means to abolish the mutagenicity. Some ‍brands of commercial bottled waters may also contain mutagens which may be derived from tap water. ‍     

Acrolein mutagenicity in the V79 assay

The mutagenicity of acrolein, allyl alcohol, glycidol and propionaldehyde was measured in V79 cells as resistance to 6-thioguanine. Acrolein was tested with and without fetal bovine serum (FBS) (10%; v/v) during the 2 h incubation period. The concentration of FBS did not affect acrolein toxicity but its mutagenicity declined as the concentration of FBS in the medium rose. Allyl alcohol (AA) was as mutagenic as acrolein (ACR). Glycidol was less mutagenic than AA and ACR. Propionaldehyde was not mutagenic at 1 microM; it was toxic at 2 microM. The data suggest that the mutagenicity of these compounds is mediated by their bifunctional nature whereas their cytotoxicity is mediated by the aldehyde function.