致癌剂

zhì ái jì
  • carcinogenic agent
致癌剂致癌剂
  1. 环境致癌剂与p53基因突变

    Environmental carcinogens and p53 gene mutation

  2. 电离辐射及化学致癌剂(BP)诱发鼠胚培养细胞姊妹染色单体互换及染色体畸变的研究

    Sister chromatid exchanges ( sce ) and chromosomal aberrations of cultured cells of mouse embryo induced by ionizing radiation and chemical carcinogen

  3. 甲醛(FA)是一种诱变剂,同时也是一种人类的可疑致癌剂。

    It is well known that formaldehyde ( FA ) is a mutagen and mammalian carcinogen .

  4. 上述结果说明,C3H/10T(1/2)细胞对研究致癌剂诱发体外培养细胞的恶性转化是有用的。

    The above results suggest that C_3H / 10T ( 1 / 2 ) cell line is very useful for the study of malignant transformation of cells in vitro induced by carcinogens .

  5. 大肠粘膜细胞色素P450在致癌剂活化中的作用及其诱导和抑制

    Role of colon mucosa cytochrome P450 in activation of carcinogen and their induction and inhibition

  6. 致癌剂DEN、促癌剂巴豆油对大鼠肝α1抑制因子3基因表达的影响

    Effects of Carcinogen DEN and Tumor Promoter Croton Oil on Rat Liver Alpha 1 - Inhibitor 3 Gene Expression in vivo

  7. 目的:探讨蛙皮素在化学致癌剂N鄄甲基鄄N'鄄硝基鄄N鄄亚硝基胍(MNNG)诱发人胃黏膜上皮永生细胞系GES鄄1癌变过程中的作用。

    Aims : To investigate the effects of bombesin on the malignant transformation of immortalized human gastric epithelial cell line GES-1 induced by chemical carcinogen N-methyl-N ′ - nitro-N-nitrosoguanidine ( MNNG ) .

  8. 方法Wistar大鼠46只,采用选择性左肺叶下部支气管灌注致癌剂3-甲基胆蒽(MCA)碘油法诱发气道上皮鳞状化生,以10只正常大鼠为对照。

    Methods 3-methylcholanthrene ( MCA ) were instilled selectively into the lower left lobe through bronchus to induce squamous metaplasia in 46 Wistar rats , and 10 normal rats served as controls .

  9. 用缺锌饲料饲养Wister大鼠,以N-甲基-N硝基-N亚硝基胍(MNNG)作为致癌剂染毒,观察了缺锌对大鼠的危害。

    The harms on the Wister rats fed by zinc-deficiency feed were observed when the carcinogenic substance MNNG ( C_2H_5N_5O_3 ) is used .

  10. 结论:蛙皮素可与化学致癌剂协同促进正常上皮细胞癌变,其机制可能与cyClinD1的过表达有关。

    Conclusions : Bombesin seems to exert a synergistic effect with chemical carcinogen in promoting malignant transformation of normal epithelial cells , which may be related to the increased cyclin D1 expression .

  11. 目的:绿茶提取物GTC对用致癌剂DMBA诱发的SD大鼠乳腺增生性病变的抑制作用。

    Objective : To illustrate the inhibitory effect of GTC ( green tea catechins ) on the development of the hyperplastic lesions in rat mammary gland induced by DMBA .

  12. 本研究旨在观察致癌剂MMS对酿酒酵母S288C细胞DNA损伤反应以及对端粒酶活性的影响,为端粒酶与恶性肿瘤的关系提供科学依据。

    Our aim was to investigate the effect of carcinogen MMS on DNA and telomerase activity of S.cerevisiae S288C and provide some scientific foundation for the relation between telomerase and cancer .

  13. 目的:探讨外源性血管内皮细胞生长因子(VEGF)对致癌剂N-nitroso-N-methylurea(NMU)诱导Copenhagen(COP)大鼠乳腺癌发生的影响。

    Objective To study the effects of extraneous vascular endothelial growth factor ( VEGF ) on mammary carcinogenesis in resistant Copenhagen ( COP ) rats induced by N-nitroso-N - methylurea ( NMU ) .

  14. SCE频率分析是研究环境诱变剂和致癌剂引起人类遗传物质损伤的有效手段。

    The analysis of Sister Chromatid Exchanges ( SCE ) frequencies is a useful tool for the study of damages in genetic material of human beings induced by environmental mutagens and carcinogens .

  15. 鼻咽癌患者外周淋巴细胞经紫外线或化学致癌剂N-甲基-N'-硝基-N-亚硝基胍(MNNG)处理后,其非程序DNA合成(UDS)值比健康人的为低;

    Using UV or MNNG as inducing agents , the UDS values of peripheral lymphocytes from patients with nasopharyngeal carcinoma ( NPC ) were found to be lower than that from normal healthy subjects .

  16. 目的考察金复康对给予致癌剂DMH(二甲肼)后大鼠结肠肠腺细胞增殖和凋亡动力学特性的影响。

    Objective : To study the effect of JinFuKang in rat colonal crypt mitosis and apoptosis cell kinetics after exposure to DMH , a carcinogen .

  17. 目的观察硒对致癌剂氧化偶氮甲烷(AOM)所致大鼠结肠癌形成过程中,垂体远侧部ACTH阳性细胞的影响。

    Objective To observe the effect of selenium on the ACTH positive cells in the pars distalis of pituitary of rat with colon mucosa cancer induced by azoxymethane ( AOM ) .

  18. 方法:1.取体重150~200g雄性近交系F334大鼠150只,随机分为实验组和对照组,利用化学致癌剂二乙基亚硝胺(DEN)建立起近交系F334大鼠肝癌模型。

    150 male inbred rats ( 75-100Kg ) are divided into experimental group and control group randomly , the rat of liver cancer model is established by low dose DEN . 2 .

  19. 世界卫生组织以及国际癌症研究机构都将砷列为人类的致癌剂,在USEPA列表中砷也被认为是1号毒素。

    World Health Organization and International Agency for Research on Cancer has classified arsenic as a carcinogen , arsenic has been regard as the most toxic substance by the USEPA as well .

  20. 结论:化学致癌剂诱发实验性早期肝癌过程中,IL6可能是激活HGF的细胞因子,HGF以自分泌机制发挥促肝细胞增殖的效用。

    Conclusions During rats are induced into early hepatocellular carcinomas by chemical carcinogen , the gene of HGF may be actived by a cytokine , IL 6 . An autocrine mechanism was suggested in HGF for the proliferation of hepatocytes .

  21. 化学致癌剂和化学致癌机理的研究状况

    Situation for Researches on Chemical Carcinogens and on Mechanism of Chemical Carcinogenesis

  22. 化学致癌剂诱发大鼠肝癌过程中凝集素受体的表达

    The expression of lectin receptors during hepatocarcinogenesis induced by chemical carcinogen in rats

  23. 本实验以二甲肼[1,2-Dimethylhydrazine,DMH]为致癌剂诱发大鼠大肠癌。

    The ultrastructure of the 1,2-dimethylhydrazine ( 1,2-DMH ) induced colorectal carcinoma was studied in rats .

  24. 对比主流烟,侧流烟具有较高浓度的致癌剂;

    The sidestream smoke has higher concentrations of cancer-causing agents ( carcinogens ) than the mainstream smoke .

  25. 目的大量研究证实导管样复合体就是胰腺癌的前体病变,因此,本研究旨在探索植入致癌剂后胰腺癌前体病变的产生和发展。

    Objective To identify the changes that produce the precursor lesions immediately after implantation of carcinogen and investigate their development .

  26. 这些平面扁平环形化合物能插入细胞的核酸中并且充当移码突变剂和致癌剂。

    These flat-ringed planar compounds intercalate with the cells ' nucleic acids . and act as frameshift mutagens and carcinogens .

  27. 结论在致癌剂作用下所出现的卵圆细胞及其分化的过渡细胞,与肝癌细胞具有某些共同的糖结合蛋白。

    Conclusion Oval cells induced by carcinogen , and transitional cells derived from oval cells share the same glycoproteins with HCC ;

  28. β-连环素及其相关蛋白在致癌剂引起的大鼠气道上皮鳞状化生中的表达

    Expression of β - catenin and Its Related Proteins in Squamous Metaplasia of Airway Epithelium Induced by Carcinogen in Wistar Rats

  29. 本文综述了化学致癌剂及化学致癌机理的近代研究状况。

    The recent situation for the researches on chemical carcinogens and on the mechanism of chemical carcinogenesis is reviewed in this paper .

  30. 近来作者提出了化学致癌剂结构与活性关系的定量分子轨道模型&双区理论。

    Recently , the author of this paper has suggested a quantitative molecular orbital model & " di-regions theory " for the chemical structure-carcinogenic activity relationship .