辐射后淋巴细胞的G显带染色体畸变分析

目的:通过染色体G显带技术研究辐射后染色体的结构畸变情况。方法:4MV的X线辐射离体入血,淋巴细胞培养后,应用染色体G显带技术,分析辐射后染色体的结构畸变情况,包括双着丝粒、缺失、易位、环状染色体、染色体片段,等。结果:辐射后观察分散良好、形态清晰的细胞核型100个,染色体畸变总数为428,其中双着丝粒、缺失、易位、环状染色体、染色体片段的发生数分别为86、41、111、9、181。分析各号染色体辐射后畸变情况,未见明显差异。结论:染色体G带分析可以提供较丰富的染色体结构畸变信息。     

辐射后淋巴细胞的G显带染色体畸变分析

目的：通过染色体G显带技术研究辐射后染色体的结构畸变情况。方法：4MV的X线辐射离体入血,淋巴细胞培养后,应用染色体G显带技术,分析辐射后染色体的结构畸变情况,包括双着丝粒、缺失、易位、环状染色体、染色体片段,等。结果：辐射后观察分散良好、形态清晰的细胞核型100个,染色体畸变总数为428,其中双着丝粒、缺失、易位、环状染色体、染色体片段的发生数分别为86、41、111、9、181。分析各号染色体辐射后畸变情况,未见明显差异。结论：染色体G带分析可以提供较丰富的染色体结构畸变信息。     

辐射剂量和染色体不稳定畸变的量效关系

目的:探讨辐射剂量和染色体不稳定畸变的量效关系.方法:应用4MV X线对离体淋巴细胞进行0、0.5、1、2、3、4、5、6Gy的辐射.进行淋巴细胞培养3天后,染色体分析,计数100个细胞的双着丝粒、着丝粒环、无着丝粒断片.统计分析辐射剂量和畸变染色体数目的量效关系.结果:0、0.5、1、2、3、4、5、6Gy的辐射后染色体畸变发生率为0%、6%、15%、41%、72%、148%、231%、382%,拟合曲线为Y=12.582X2 -15.387X+9.715.结论:染色体不稳定畸变发生率随辐射剂量增加呈二次多项式关系增加.     

辐射剂量和染色体不稳定畸变的量效关系

目的：探讨辐射剂量和染色体不稳定畸变的量效关系。方法：应用4MVX线对离体淋巴细胞进行0、0．5、1、2．3、4、5、6Gy的辐射。进行淋巴细胞培养3天后,染色体分析,计数100个细胞的双着丝粒、着丝粒环、无着丝粒断片。统计分析辐射剂量和畸变染色体数目的量效关系。结果：0、0．5、1、2、3、4、5、6Gy的辐射后染色体畸变发生率为0％、6％、15％、41％、72％、148％、231％、382％,拟合曲线为Y=12．582X^2-15．387X＋9．715。结论：染色体不稳定畸变发生率随辐射剂量增加呈二次多项式关系增加。     

78例急性白血病患儿的G显带染色体分析

对78例急性白血病患儿的骨髓细胞进行G显带染色体分析结果是:染色体数目异常,以亚二倍体为主,伴有假二倍体及超二倍体;染色体结构异常,大部分见于急非淋白血病。在36例急非淋白血病中,16例有染色体异常核型,占44.4％;在42例急淋白血病中,1例有异常核型,仅占2.4％。     

丝裂霉素C诱发染色体畸变的量效关系与特异性断裂点的观察

采用全血培养的方法,观察MMC诱发染色体畸变。结果表明,染色体断裂频率与MMC浓度呈直线正相关;畸变细胞率与MMC浓度的对数呈直线正相关;染色体畸变类型较多见染色单体交换;畸变较集中地发生于着丝粒部位;非着丝粒部位的畸变倾向于发生在含有脆性部位的染色体区带。     

上海"6.25"辐射事故受照者14年染色体畸变随访研究

背景与目的:1990年上海"6.25"60co源辐射事故中2例重度、3例中度骨髓型急性放射病患者被救治成功.为了阐明放射病的远后效应,对该5名受照者连续进行照后14年的染色体畸变随访观察,为辐射远后效应评价积累资料.材料与方法:常规染色体畸变分析、G-显带自动核型分析以及用全染色体涂染探针进行FISH分析,检测非稳定性畸变(Cu)和稳定性畸变(Cs),并将历年检测结果进行比较.结果:照后3.5年染色体Cu畸变降至初始水平的20%左右,照后14年已基本丢失贻尽.残留的畸变以易位等Cs畸变为主.cs与复杂畸变的出现频率均与受照剂量相关,照后6～14年基本保持不变.G-显带自动核型分析与FISH方法检出的总畸变率大体一致.各条染色体的断裂几率呈随机分布.染色体畸变的恢复速度及远后效应的严重程度不仅与受照剂量有关,而且与机体的健康状况密切相关.结论:Cs畸变是评价辐射远后效应的理想指标.对事故受照者进行长期随访观察具有十分重要的意义.     

鼻咽癌患者染色体端粒联合与染色体畸变关系的研究

为了探讨鼻咽癌染色体端粒联合与染色体畸变的关系,采用Ｇ显带技术,对２５例鼻咽癌患者外周血的染色体端粒联合频率进行观察,同时与染色体畸变的关系进行了分析。结果表明：鼻咽癌患者染色体端粒联合频率（３５．０７％）及染色体畸变率（１２．３３％）均显著高于对照组（２０．２７％及２．４６％）,２者有非常显著性差异（Ｐ＜０．０１）。端粒联合的位点与染色体畸变断裂点在染色体上的分布密切相关（γ＝０．８１４９,Ｐ＜０．０５）,说明染色体端粒联合发生是染色体畸变形成的机理之一。     

P-32持续低剂量率辐射对外周血淋巴细胞染色体的损伤研究

目的:探讨P-32持续低剂量率辐射对外周血淋巴细胞的染色体损伤.方法:应用不同活度(0、0.01、0.1、0.5、2.7MBq)的放射性P-32胶体溶液,加入6ml的外周血淋巴细胞培养液中,培养3天后进行染色体分析.结果:0.01、0.1、0.5 MBq的P-32持续低剂量率辐射均造成染色体不稳定畸变(双着丝粒、着丝环、无着丝粒断片),随放射性活度增加而增加;2.7MBq的P-32辐射剂量较大,染色体形成率很低.结论:0.01、0.1、0.5 MBq的P-32持续低剂量率辐射可以造成染色体不稳定畸变,随辐射剂量增加畸变率增加;2.7MBq P-32的辐射剂量过大,染色体形成率很低不利于染色体畸变分析.     

人外周血淋巴细胞高分辨染色体制备技术的研究

目的： 建立一种具有分裂指数高和染色体分散好等优点的550~850条带纹高分辨染色体的制备方法。方法：取10例健康人外周血为样本制备淋巴细胞高分辨染色体。固定5-氟尿嘧啶核苷、尿嘧啶核苷、胸腺嘧啶核苷、溴化乙锭、秋水仙胺的剂量,进行5个因素3个水平的正交设计15种实验方案。5个因素分别为培养时间、胸腺嘧啶核苷、溴化乙锭、秋水仙胺作用时间以及低渗时间。3个水平分别为培养时间64、72、80 h;胸腺嘧啶核苷作用时间16、17、18 h;溴化乙锭作用时间3、4、5 h;秋水仙胺作用时间10、15、20 min以及低渗时间30、40、50 min。每例样本同时采用15种方案进行实验,比较各方案带纹在550条以上时染色体分裂指数和分裂相分散的情况。结果：在15种方案中培养时间以及秋水仙胺作用时间对分裂指数有显著影响 (P＜0. 01),其中培养72 h后加5-氟尿嘧啶核苷和尿嘧啶核苷进行同步化和秋水仙胺作用15 min高分辨染色体分裂指数最大。37 ℃低渗40 min高分辨染色体分散效果最佳。结论：本实验方案的高分辨染色体制备方法,具有分裂指数高和染色体分散好等优点,具有较好的推广价值。     

基于八腔室玻片的染色体畸变初筛方法的建立与验证

目的：为简化传统体外染色体畸变试验工序并减少受试物用量,建立基于八腔室玻片的染色体畸变初筛方法。方法：首先利用环磷酰胺（CP）和丝裂霉素C（MMC）作为阳性模式药物,分别建立CP作用6 h（＋S_9）和MMC作用24 h（-S_9）的八腔室玻片的染色体畸变试验方法。再用于检测5个已知遗传毒性物质苯并芘[B（a）P]、2-氨基蒽（2-AA）、甲基磺酸甲酯（MMS）、乙基磺酸甲酯（EMS）、依托泊苷（Eto）和2个非遗传毒性药物氨苄青霉素钠（AS）和氯化钠（SC）在±S_9两个条件下的染色体畸变效应,验证该法的灵敏度和特异性。结果：CP和MMC分别在±S_9活化系统中染色体结构畸变率呈浓度依赖性增加,与溶剂对照组相比,差异均具有统计学意义（P〈0.05或P〈0.01）。在验证试验中,B（a）P和2-AA在＋S_9系统中呈染色体畸变阳性,与溶剂对照组相比,差异均具有统计学意义（P〈0.05或P〈0.01）;MMS、EMS和Eto的染色体畸变率呈浓度依赖性增加（±S_9结果均为阳性）,与溶剂对照组相比,差异均具有统计学意义（P〈0.05或P〈0.01）;而2个已知非遗传毒性药物（AS和SC）在±S_9系统中均呈阴性结果。结论：通过上述物质的验证表明,八腔室玻片染色体畸变试验是一种简单、快速、有效的遗传毒性初筛方法。     

Non-random structural chromosomal changes in ovarian cancer: i(5p) a novel recurrent abnormality

Ovarian cancer represents the leading cause of death among patients with gynecological cancer. The genetic changes underlying the initiation and progression of ovarian cancer have not been well defined. However, non-random structural chromosomal changes have been identified with common chromosomal breakpoints. We have studied cytogenetically 15 cases of ovarian adenocarcinomas by a direct culture of cancer cells and a G-banding technique investigating the presence of recurrent structural aberrations with common chromosomal breakpoints. Among very complex structural rearrangements found, we could recognize recurrent structural aberrations involving according to frequency chromosomal regions 3p13-14, 11p15, 19q13, 3q21, 11q23, 11q10, 1p13, 1p36, and 17q24-25. Isochromosomes i(5p), i(17q), i(8q) and i(11q) were also observed. Isochromosome i(5p), rarely reported in ovarian cancer was found in seven cases suggesting that it may be a novel recurrent abnormality. Translocations t(1;11), t(3;19), t(3;17), t(7;11) and t(11;17) were also identified. Conventional cytogenetics continues to be valuable detecting the presence of non-random chromosomal breakpoints and facilitating the identification of genes implicated in tumorigenesis.     

Unequivocal evidence of genotoxic potential of argemone oil in mice

Consumption of mustard oil adulterated with argemone oil leads to a clinical condition, commonly referred to as "Epidemic Dropsy." Since in vitro studies have shown that sanguinarine, an active benzophenanthridine alkaloid of argemone oil, intercalates DNA molecule, the in vivo clastogenic and DNA damaging potential of argemone oil was investigated in mice. Swiss albino mice were intraperitoneally administered 0.5, 1.0, 2.0 and 4.0 ml/kg body wt. of argemone oil to analyze chromosome aberrations and micronucleus test, while 0.25, 0.5, 1.0 and 2.0 ml/kg body wt. were given for alkaline comet assay. The frequencies of chromosomal aberrations and micronucleated erythrocytes formation in mouse bone marrow cells increased in a dose-dependent manner following argemone oil treatment. However, significant induction in chromosomal aberrations (83%) and micronucleated erythrocytes formation (261%) were observed at a minimum dose of 1.0 ml/kg. The results of comet assay revealed DNA damage in blood, bone marrow and liver cells following argemone oil treatment. Olive tail moment (OTM) and tail DNA showed significant increase in bone marrow (35-44%) and blood cells (25-40%) even at a dose of 0.25 ml/kg body wt. of argemone oil. In liver cells, OTM was significantly increased (20%) at a dose of 0.25 ml/kg, while all the comet parameters including OTM, tail length and tail DNA showed significant increase (31-101%) at a dose of 0.5 ml/kg. These results clearly suggest that single exposure of argemone oil even at low doses produces genotoxic effects in mice.     

Clonal chromosomal aberrations in simian virus 40-transfected human thyroid cells and in derived tumors developed after in vitro irradiation.

In vitro model cell systems are important tools for studying mechanisms of radiation-induced neoplastic transformation of human epithelial cells. In our study, the human thyroid epithelial cell line HTori-3 was analyzed cytogenetically following exposure to different doses of alpha- and gamma-irradiation and subsequent tumor formation in athymic nude mice. Combining results from G-banding, comparative genomic hybridization, and spectral karyotyping, chromosome abnormalities could be depicted in the parental line HTori-3 and in nine different HTori lines established from the developed tumors. A number of chromosomal aberrations were found to be characteristic for simian virus 40 immortalization and/or radiation-induced transformation of human thyroid epithelial cells. Common chromosomal changes in cell lines originating from different irradiation experiments were loss of 8q23 and 13cen-q21 as well as gain of 1q32-qter and 2q11.2-q14.1. By comparison of chromosomal aberrations in cell lines exhibiting a different tumorigenic behavior, cytogenetic markers important for the tumorigenic process were studied. It appeared that deletions on chromosomes 9q32-q34 and 7q21-q31 as well as an increased copy number of chromosome 20 were important for the tumorigenic phenotype. A comparative breakpoint analysis of the marker chromosomes found and those observed in radiation-induced childhood thyroid tumors from Belarus revealed a coincidence for a number of chromosome bands. Thus, the data support the usefulness of the established cell system as an in vitro model to study important steps during radiation-induced malignant transformation in human thyroid cells.     

草苔虫内酯的遗传毒性评价

目的：检测草苔虫内酯的遗传毒性。方法：采用Ames试验、体外培养中国仓鼠卵巢（chinese hamsterovary,crto）细胞染色体畸变试验和小鼠骨髓微核试验检测草苔虫内酯的遗传毒性。结果：Ames试验显示在每皿100、10、1、0．1g受试剂量下,在加或不加S9代谢活化系统时对组氨酸缺陷型鼠伤寒沙门氏菌TA97、TA98、TA100、TA102及TAl535所诱发的回复突变菌落数均与溶剂对照的突变菌落数相近。体外培养CHO细胞染色体畸变试验结果显示,在3．75、1．88和0．94g／ml 3个剂量组,在加S9条件下培养24h和不加S9培养24、48h的CHO细胞染色体畸变率与溶剂对照组相比差异有统计学意义（P〈0．05）。小鼠骨髓微核试验,在12．5、25、50g／kg3个剂量下对ICR小鼠的微核诱发率呈剂量反应关系,与溶剂对照组相比差异有统计学意义（P〈0．01）。结论：在本实验条件下,草苔虫内酯对鼠伤寒沙门氏菌无致突变性,对哺乳动物培养细胞染色体的致畸变作用为可疑阳性,对ICR／b鼠有诱发骨髓嗜多染红细胞微核的效应,提示草苔虫内酯对人体具有潜在的遗传毒性。