丹参对丝裂霉素C诱发小鼠生殖细胞遗传损伤的防护作用研究

本文根据动物实验模型的设计，研究了中药丹参对丝裂霉素Ｃ（ＭＭＣ）诱发雄性小鼠过生殖细胞遗传损伤的防护效应。雄性昆明小鼠随机分成８组，每组１５只，实验组分别注射高、中、低剂量丹参和ＭＭＣ，观察动物的精子畸形率、早期精细胞微核率和精原细胞染色体畸变率。结果表明，中药本身无诱变损伤作用，而对ＭＭＣ有拮抗抑制作用。提出中药丹参具有抗ＭＭＣ诱发小鼠生殖细胞遗传损伤的作用。     

11种天然药材及植物的抗突变与致突变同步试验报告

本文报告用ＳＯＳ噬菌体诱导试验的抗突变与致突变同步试验法，对１１种天然中药及植物甘草、枸杞、半枝莲、柴胡、丹参、黄芪、决明子、仙人球、仙人指、胡萝卜及青萝卜的抗突变及致突变性进行了筛检。经过加和不加大鼠肝微粒体酶代谢活化系统（Ｓ９）的２种试验及重复验证，结果１１种中药及植物均未发现致突变作用，甘草、枸杞、丹参、黄芪、胡萝卜、青萝卜及仙人指可抑制抗肿瘤药物丝裂霉素Ｃ（ＭＭＣ）的致突变性。     

五加皮的体内抗诱变性研究

本文采用小鼠髓嗜多染红细胞微核试验和小鼠精子畸形试验，探讨中药五加皮的体内抗诱变作用。结果表明，五加皮各剂量（１ｇ／ｋｇ，２ｇ／ｋｇ，４ｇ／ｋｇ，４ｇ／ｋｇ）对ＭＭＣ诱发的微核率和精子畸形率均有明显的拮抗作用（Ｐ〈０．０１），微核抑制率达５０．５％、７３．２７％，精子畸形抑制率高达７３．４５％、８４％。结果显示，五加皮具有拮抗ＭＭＣ诱发的体细胞和生殖细胞遗传损伤的作用。     

STUDY ON THE ANTIMUTAGENIC EFFECT IN VIVO OF CORTEX ACANTHOPANASIA RADICIS

本文采用小鼠骨髓嗜多染红细胞微核试验和小鼠精子畸形试验,探讨中药五加皮的体内抗诱变作用。结果表明,五加皮各剂量（１ｇ／ｋｇ,２ｇ／ｋｇ,４ｇ／ｋｇ）对ＭＭＣ诱发的微核率和精子畸形率均有明显的拮抗作用（Ｐ＜０．０１）,微核抑制率达５０．５％－７３．２７％,精子畸形抑制率高达７３．４５％－８４％。结果提示,五加皮具有拮抗ＭＭＣ诱发的体细胞和生殖细胞遗传损伤的作用。     

生物反应调节剂（BRM－102）冲剂诱变和抗诱变作用的研究

采用微核法对生物反应调节剂冲剂（ＢＲＭ－１０２）的诱变和抑制诱变作用进行了研究。结果显示ＢＲＭ－１０２提取液各种浓度组与阴性对照组统计学处理无意义，表明该冲剂尚未有诱发正常人淋巴细胞微核率升高的作用，不致引起体细胞遗传损伤；对诱变剂丝裂霉素Ｃ诱发正常人淋已细胞微核率有明显的抑制作用。     

生源健身茶的诱变性与抗诱变性研究

生源健身茶的诱变性与抗诱变性研究黄晓沐，刘茜，赵恒奎，蒋家（安徽省卫生防疫站２３００６１）为研究以绿茶为主料，在其中加入山渣、枸杞子、决明子等中药所配的生源健身茶是否能诱发遗传物质的损伤，或具有抗诱变作用，采用了小鼠骨髓细胞微核试验进行生源健身茶的诱...     

人胚细胞提取物拮抗环磷酰胺诱发小鼠骨髓微核的研究

本文研究了人胚细胞提取物（胚提物）对小鼠自发和环磷酰胺（ＣＰ）诱发骨髓嗜多染细胞（ＰＣＥ）微核的影响．结果表明：①胺腔注射０．３，３和３０ｍｇ／ｋｇ．体重的胚提物，小鼠骨髓ＰＣＥ微核率（ＭＮＦ）与对照组相比无显著差异．②ＣＰ可诱发ＰＣＥ的ＭＮＦ显著增加（Ｐ＜０．０１）．③注射ＣＰ和上述剂量的胚提物，可使ＭＮＦ呈剂量依赖性下降，当剂量达３和３０ｍｇ／ｋｇ．体重时，ＭＮＦ下降显著（Ｐ＜０．０５和＜０．０１）．上述结果提示；胚提物无诱发小鼠骨髓微核作用，而对ＣＰ诱发小鼠ＰＣＥ微核则有拮抗作用，这一结果在临床肿瘤化疗上有潜在的应用价值．     

胎肌条件培养液抗损伤效应的观察

胎肌条件培养液（ＦＭＣＭ）可在ＣＦＵ－ＧＭ体外培养中提供集落刺激活性。研究发现它还能在体外培养中保护ＣＦＵ－ＧＭ，减轻理化损伤因素对其生长的抑制效应。所用化学损伤因素为５×１０－７Ｍ的阿糖胞苷与９×１０－９Ｍ的三尖杉酯碱，物理损伤因素为放射（３．５Ｇｙ），热（４４℃，６０分钟）与冷（—２０℃，１６分钟）。在损伤因素作用下，ＣＦＵ－ＧＭ的集落产率受到明显抑制，用２０％ＦＭＣＭ处理后，抑制现象可以减轻。ＦＭＣＭ可以对抗多种因素对ＣＦＵ－ＧＭ的抑制作用，没有特异性。用胰蛋白酶或热（８５℃，３０分钟）处理后的ＦＭＣＭ不具上述保护效应，用酸（ＰＨ＝２），碱（ＰＨ＝１０），ＤＮＡ酶与透析处理则无明显影响。提示ＦＭＣＭ中起保护作用的活性物质可能为分子量大于１００００的蛋白质。     

胎盘免疫调节多肽遗传毒性和抗突变作用的研究

本语文应用体外培养人淋巴细胞并进行微核、染以体畸变的检测以及小鼬有髓微核实验的研究，评价胎盘免疫调节肽遗传毒性和抗突变效应，实验结果表明，胎盘免疫肽可显著抑制培养人淋巴细胞的自发和γ射线诱发的微核形成以及丝裂霉素Ｃ（ＭＭＣ）诱发的染色体畸变，并能明显抑制环磷酰胺诱发的小鼠骨髓多染性红细胞微核的增加，揭示了胎盘免疫调节肽具有抗突变作用。     

低剂量电离辐射和低浓度丝裂霉素C诱导小鼠生殖细胞交叉耐受性

本文研究了Ｘ射线与丝裂霉素Ｃ之间的交叉耐受性。首先用低剂量Ｘ射线（０．０５Ｇｙ，剂量率：０．０５Ｇｙ／ｍｉｎ）给小鼠全身均匀照射，３小时后腹腔注射损伤剂量的ＭＭＣ，对照组只给损伤剂量的ＭＭＣ；反过来，给小鼠低剂显ＭＭＣ，２４小时后，再给损伤剂量的ｘ射线（１．５Ｇｙ，剂量率：０．２９Ｇｙ／ｍｉｎ）照射，对照组注入等量的生理盐水，然后照射损伤剂量的ｘ射线。比较实验组和对照组的初级精母细胞染色体畸变率，结果发现ｘ射线与丝裂霉素Ｃ之间存在交叉耐受性。     

苏木抑制诱变效应的初步研究

在丝裂霉素(MMC)诱导下,生长中细胞的姊妹染色单体互换频率显著增高,环磷酰胺(C.C.P)可诱发高微核率,已被普遍认同。本文以SCE及微核率为检测指标,观察活血化瘀药物:“苏木”抗MMC及C.C.P的诱导。发现苏木对MMC、C.C.P的诱导有一定的抑制作用,但其本身也能致使细胞SCE升高。     

Influence of spermidine on sister chromatid exchanges induced by alkylating agents in mammalian cells in vitro

Sister chromatid exchanges (SCEs) are a very sensitive genetic end-point for in vitro identification of presumed carcinogenic and mutagenic agents, although the mechanism of their formation is still to be elucidated. The present work shows the influence of spermidine on SCE induction by two different DNA damaging agents: Mitomycin-C (MMC) and N-Methyl-N'-Nitro-N-Nitrosoguanidine (MNNG). The SCE level induced by MMC was significantly decreased by spermidine. On the contrary, MNNG-induced SCEs were not affected. It has recently been suggested that MMC, via its reduced metabolite mitosene, produces bulky mono-and bi-adducts in DNA, mainly located in the minor groove of the double helix. MNNG, instead, directly methylates several electrophilic sites of DNA bases, such as the N7 and the O6 of guanines and the N3 of adenines. Both MMC and MNNG, despite their different mechanism of action, are potent SCE inducers. Spermidine, similarly to its structural analogue Spermine, is known to interact with DNA phosphate groups and to bind reversibly to the minor groove, thus stabilizing the double helix structure. Spermidine, being therefore ineffective on the MNNG-mediated DNA methylation, might affect DNA, making it structurally unavailable for MMC binding.     

康尔爱胶囊抗突变的实验研究

目的 :观察康尔爱胶囊对环磷酰胺诱发的微核 (MN)和姐妹染色单体互换 (SCE)的抑制作用及对人胃腺癌SGC 790 1细胞突变型p5 3基因表达的影响。方法 :以ICR纯种小鼠的骨髓细胞为材料 ,以微核及姐妹染色单体互换为指标 ,研究康尔爱胶囊的致变、抗变作用 ;以人胃腺癌SGC 790 1细胞为材料 ,应用流式细胞仪检测康尔爱胶囊对人胃腺癌SGC 790 1细胞突变型p5 3基因表达的抑制作用。结果 :康尔爱胶囊 3个剂量组微核率及SCE数与阴性对照组比差异均无显著意义 ;康尔爱胶囊 3个剂量组对环磷酰胺诱发的微核及引起的SCE升高均有明显的抑制作用 ;康尔爱胶囊 3个剂量组突变型p5 3基因表达与阴性对照组比差异显著。结论 :康尔爱胶囊无致变作用且有一定的抗变作用 ;康尔爱胶囊对突变型p5 3基因表达有一定的抑制作用     

几味中药复方提取液对正常的和丝裂霉素C诱发的淋巴细胞微核率的影响

将茜草、淫羊藿、人参组成复方，提取其水溶成分，观察其对正常的淋巴细胞和用丝裂霉素Ｃ（ＭＭＣ）诱发的淋巴细胞的微核率的影响。结果表明，各种浓度的提取液，诱发正常淋巴细胞微核不同，随着浓度的增高，微核率有上升趋势。而对ＭＭＣ诱发淋巴细胞微核的影响不显著。Ｐ＞００５。     

Genetic etiology of esophageal cancer--III. The spontaneous and mitomycin-C (MMC) induced sister chromatid exchanges (SCE) and chromosome aberrations in cultured lymphocytes from members of "high risk" and "low risk" esophageal cancer families in Linxian County

The spontaneous and mitomycin-c (MMC) induced sister chromatid exchanges (SCE) and chromosome aberrations in cultured lymphocytes from members of "high risk" and "low risk" esophageal cancer families in Linxian County were studied. The results showed that the frequencies of the spontaneous SCE of "high risk" and "low risk" esophageal cancer groups were 7.8 +/- 0.25 and 8.3 +/- 0.25/per cell. There were no difference between these two groups (P greater than 0.5). The frequencies of the SCE induced by MMC in "high risk" and "low risk" esophageal cancer groups were 43.8 +/- 2.4 and 21.6 +/- 1.1/per cell. There were noteworthy difference (P less than 0.001). However, the frequencies of the spontaneous and MMC induced chromosome aberrations in "high risk" cancer families were higher than those of the "low risk" ones.     

改良的人淋巴细胞微核试验检测非整倍体诱发剂的研究

为了快速检测非整倍体诱发剂，我们应用体外培养淋巴细胞微核检测法，根据非整倍体诱发剂与染色体断裂诱发的微核形成于不同的细胞周期来评估非整倍体诱发剂，结果表明，（１）非整倍体诱发剂ＶＣＲ与染色体断裂剂ＭＭＣ相比，在药物处理后７小时引起微核率显著上升；（２）与对照组相比，ＶＣＲ处理后５，７ｈ引起微核率显著性升高，以７ｈ的微核出率最高；而ＭＭＣ处理组在处理后各个时间的微核率与对照组相比均无显著性差异。本实     

多细胞系胞质分裂阻滞微核细胞组学试验法的建立与应用

目的: 采用不同组织来源的细胞系建立微核细胞组学,比较其遗传毒性生物标志物的敏感性,并研究雷公藤甲素(TPL)和甘草酸二铵(DG)对大鼠成纤维肺细胞(CHL)和犬肾小管上皮细胞系(MDCK)细胞微核率的影响。方法:首先建立方法,采用不同浓度丝裂霉素C(MMC)与CHL、L02、MDCK、Bhas42细胞作用6 h后给予细胞松弛素B(CytoB)继续培养约1.5个细胞倍增时间。收获细胞、制片、染色及镜检。计算每个剂量胞质分裂增殖指数(CBPI)、复制指数(RI)、坏死(Nec)及凋亡(Apop)细胞的千分率、双核细胞中微核(MN)、核芽(NBUD)和核质桥(NPB)出现的千分率。然后进行方法的验证,采用CHL细胞经不同浓度(1、10和100 μg/mL)DG预处理24 h后观察DG对上述细胞毒性和微核细胞组相关指标的影响。为进一步了解微核细胞组学对遗传毒性靶器官评估的效果,MDCK细胞经DG(10 μg/mL)预处理24 h后采用不同浓度(1和5 μg/mL)TPL染毒1 h,观察其对遗传毒性的影响。结果:MMC诱发的不同细胞系细胞毒性(CBPI、RI、Apop与Nec)均随MMC浓度升高呈升高趋势。各组细胞的MN、NBUD和NPB均出现不同程度的剂量相关性升高,但不同细胞系对MMC诱发的生物标志物峰值出现的敏感度不同。在验证实验中,与对照组相比,DG(10和100 μg/mL)对MMC(0.2 μg/mL)诱发的MN、NBUD和NPB升高有显著的抑制作用(P均<0.05)。TPL可诱发MDCK细胞NBUD和MN显著上升(P<0.05),且DG预处理可有效拮抗该效应(P<0.05)。结论:多细胞系胞质分裂阻滞微核细胞组学实验法可同时对多项遗传毒性指标进行评价。DG对CHL及MDCK细胞产生的染色体断裂有保护作用,在临床配伍中可发挥抗细胞DNA损伤的功效。     

Persistence of sister chromatid exchanges and in vitro morphological transformation of Syrian hamster fetal cells by chemical and physical carcinogens

The induction of neoplastic cell transformation is closely associatedwith DNA alterations which occur shortly after carcinogen exposure.Sister chromatid exchange (SCE) formation is a sensitive indicatorof carcinogen-DNA interaction and correlates with the inductionof morphological cell transformation. The persistence of lesionsgenerating SCE produced by chemical and physical carcinogensand its relevance to the induction of morphologic transformationwas evaluated in coordinated experiments with cultured Syrianhamster fetal cells (HFC). Exponentially growing HFC were exposedfor 1 h to benzo[a]pyrene (BP), methyl-methanesulfonate (MMS),cis-platinum (II) diaminedichloride (cis Pt II), N-methyl-N'-nitrosourea(MNU), mitomycin C (MMC), N-methyl-N'-nitro-N-nitrosoguanidine(MNNG), N-acetoxy-2-fluorenyl-acetamide (AcAAF) or u.v. lightirradiated. Cells were incubated for 24 h with 5-bromodeoxyuridine(BrdUrd) required for SCE visualization at 1, 24 and 48 h aftercarcinogen exposure. The induction of morphological transformationwas determined on the quantitative colony assay at 6 days aftercarcinogen treatment. SCE analysis demonstrates that for a periodof 48 h after carcinogen exposure, during which time the cellsundergo at least four replicative cycles, DNA damage generatingSCE induced by all chemical carcinogens either persisted orwas partially removed, whereas u.v.-induced lesions were completelyremoved. An elevated SCE frequency persisted after two additionalcell cycles after treatment with BP, AcAAF or MMC without increasedcell lethality as compared to other carcinogens whose lesionswere completely eliminated during the same period. Althougha correlation between the persistence of SCE and the inductionof transformation was not observed for all carcinogens, thisstudy illustrates that DNA damage generating SCE can persistover several replicative cycles, thus raising the possibilitythat lasting DNA alterations are important for the inductionof neoplastic cell transformation.     

环磷酰胺诱发的染色体损伤与P53基因表达的关系

目的：探讨环磷酰胺(cyclophosphamide,CP)对染色体损伤与P53基因表达间的关系。　方法：以正常人外周血淋巴细胞为材料,用流式细胞仪检测环磷酰胺对突变型P53基因表达的影响,同时以微核(MN)及姐妹染色单体互换(SCE)为指标,进行致突变研究。　结果：环磷酰胺用药组突变型P53基因表达率为30.81 ％,微核率为8 ‰,姐妹染色单体互换率为9.21±1.08,与对照组比较均有显著差异。　结论：环磷酰胺的致突变作用可能与影响P53的基因的表达有关。     

培养人淋巴细胞微核测试法检测非整倍体诱变剂的研究

直接用培养人淋巴细胞微核测试系统，采取控制化学品处理培养细胞和恢复时间，对已知非整倍体诱变剂长春新碱进行微核检测，实验结果显示，在设定的微核检测程序中，阴性对照和断裂剂丝裂霉素Ｃ未诱发微核率的显著增加（Ｐ〉０．０５）而ＶＢＬ却引起ＭＮＦ显著增加（Ｐ〈０．０１）。结果揭示培养人外周血淋巴细胞微核测试法可能成为一种新的人类化学品非整倍体诱变剂的检测方法。