用紫露草微核技术检测甘蔗色素的诱变性

本文报告了用紫露草微核技术,检测甘蔗色素的诱变性。甘蔗色素是从甘蔗渣中提取出来用作食品添加剂的天然色素,在动物试验中发现它能引起小鼠精子畸变率增加。为了检测甘蔗色素对紫露草微核的诱变性,用75枝花序分为五组,分别用5、10、15mg/ml三种浓度的甘蔗色素处理,以自来水为阴性对照,5mg/ml甲醛为阳性对照,观察紫露草微核发生率,结果所有用甘蔗色     

明矾对紫露草微核的诱变效应

利用紫露草微核监测明矾的诱变效应，结果表明，明矾在１ｍｇ／ｍｌ浓度以下时，紫露草微核率与蒸馏水对照组比较差异无显著性，但当明矾浓度达到２ｍｇ／ｍｌ以上时，微核率明显高于蒸馏水对照组，并呈现剂量效应关系。说明明矾对紫露草具有较强的诱变效应。     

紫露草两种检测技术的研究

紫露草两种检测技术的研究蒋永光庾樟娣桂林市环保监测站桂林５４１００２以植物检测法检测环境中的诱变剂，具有简便、经济、快速而有效的特点，它可以综合而灵敏地反映出环境中诱变剂的存在及污染的现状。其中，紫露草检测技术是近年来研究得最多的检测方法之一。早在七...     

紫露草雄蕊毛检测法应用初探

紫露草雄蕊毛检测法应用初探蒋永光桂林市环保监测站桂林５４１００２紫露草４４３０＃雄蕊毛突变检测法比３＃微核检测法更为直观、更易于操作与统计。桂林市环保监测站承担桂林市科委下达的、用紫露草技术检测桂林市水环境诱变剂的课题，由于检测点位较多、工作量较大，...     

四种气态毒物对紫露草四分体微核及其他核异常效应的研究

用紫露草染色体畸变或微核为指标研究外界理化因素对机体的影响已有不少报导,1938年Sax首先报导了电离辐射的作用,1954年Smith又报导了化学物质作用的结果,尔后Ma TH(1967,1984))较详细和系统地报告了紫露草监测技术,并首次报导了二十多种气态毒物对紫露草四分体微核的影响。国内方宗熙(1981)报导了工业区大气污染的监测结果,董宝贤等(1984)则报告了对氯气的监测。但直到目前,大气监测远不如水体监测研究充分和系统,因而,使用上受量一定的限制,且近年来,用“核异常”这类每指标评价化学物质的影响已逐渐引起重视。因此,我们用实     

联苯胺与咖啡因对紫露草微核的敏感性试验

化学物质诱发染色体异常已有很多报导[1-3],这些物质能诱发生物遗传突变,有的致癌,与人类健康密切相关。我们选用了非水溶性致癌物联苯胺和水溶性断裂剂咖啡因[4-5],对紫露草产生微核的影响进行了比较试验,说明紫露草微核对不同类型毒物的反应具有明显差异,是一种简便而有效的     

我国紫露草生物分析方法的研究与应用概况

我国紫露草生物分析方法的研究与应用概况（上接第２期封三）４马德修,方宗熙,林光恒,等山东紫露草对诱变剂的敏感性山东海洋学院学报,１９８１;１１（４）：４７５马德修,等用紫露草微核技术对青岛某工业区空气和污水及常用农药滴滴畏（ＤＤＶ）的生物测定?..     

桂林市两工厂大气及废水的紫露草微核检测

桂林市两工厂大气及废水的紫露草微核检测蒋永光，庚樟娣，刘桂珍桂林市环保监测站桂林５４１００２１９８６年国家环保局将紫露草微核技术列为生物监测规范的方法之一。我们将此法用于桂林市Ａ、Ｂ两工厂的大气及废水的检测。实践证明，这一方法是简单、经济、快速而有效...     

紫露草微核技术监测上海石化公司某车间空气质量

紫露草微核技术监测上海石化公司某车间空气质量费建安，刘荣，姚建新，郑挂华（上海金山卫上海石化股份有限公司环保研究所２００５４０）１９９４年度，作者用紫露草微核技术监测石化行业某车间空气中甲醛质量状况。车间面积为６４５０平方米，以方格法放置８个样点。经...     

世界卫生组织化学品安全项目植物检测国际协作研究骨干会议简介

世界卫生组织化学品安全项目于1991年12月9～13日在苏联圣彼得堡召开了植物检测国际协作研究骨干会议,出席这次会议的有来自苏、美、捷、波、日、加、印、墨西哥、肯尼亚和中国等10个国家28名代表,我国广西植物研究所陈锐章研究员出席了这次会议。与会代表均在会上宣读了各自多年来在拟南芥基因突变、蚕豆微核、紫露草雄蕊毛突变和紫露草微核等四种植物检测方法的研究工作报告,经过讨论,形成一份文件,认为这四种检测方法都能有效地检测环境诱     

Trad—MCN分析中引入多微核四分体率

在Ｔｒａｄ－ＭＣＮ分析中，以微核率作指标来判断环境诱变剂对染色体的损伤程度和诱变剂量强弱一直沿用至今，本文用实验证明了当作物中存在有诱变剂镉的阻遏剂，如维生素Ｅ或褐藻酸钠时，单一微核率指标已不足以反映出诱变剂的强度与剂量大小，更不能反映诱变剂与阻遏剂间的作用及其程度，因此，作者建议应将多微核四分体率作为一项重要指标引入Ｔｒａｄ－ＭＣＮ分析中，与微核率一道共同反映在研究工作中。     

PCD检测方法的建立及其在研究外来激素对大鼠睾丸细胞PCD影响的应用

本研究1.建立了检测PCD的石蜡切片原位末端标记( ISEL ) 法, 在石蜡切片原位用免疫组化法标记核DNA,使 PCD 细胞呈黄色或棕黄色的阳性着染, 在普通光学显微镜下即可鉴别。本实验用加热和蛋白酶K同时处理背景, 使非特异性染色几乎不存在; 使用过氧化物酶—显色系统缩短时间2小时,提高了筛检DAB 速度。2.应用ISEL法研究外来激素对大鼠睾丸细胞的影响,结果发现GnRH-A是一个促凋原,具有明显的生殖毒性。     

DNA断端标记法分析HL—60和U937白血病细胞株凋亡

使用DNA断端标记法（TDT法）定量观察了白血病细胞株HL－60和U937对顺氯氨铂，羟基喜树碱，长春新碱3种抗肿瘤药物所发生的凋亡变化。HL－60对顺氯氨铂很敏感。U937对羟基树碱、长春新碱敏感。比较了核酸电泳检测的结果。并首次报道了用TDT法在荧光显微镜下可观察到细胞凋亡的三种不同形态。     

Effect of polyunsaturated fatty acids on the growth of murine colon adenocarcinomas in vitro and in vivo.

The effect of the polyunsaturated fatty acids (PUFAs) linoleic acid (LA) and arachidonic acid (AA) on the growth of two murine colon adenocarcinoma cell lines (MAC26 and MAC13) has been determined both in vitro and in vivo. When the serum concentrations in the medium became growth limiting, low concentrations (18-33 microM) of both PUFAs were growth stimulatory to both cell lines, while higher concentrations were growth inhibitory. Growth stimulation by AA in both cell lines, and by LA in MAC13, was effectively inhibited by both the cyclo-oxygenase and lipoxygenase inhibitor indomethacin, and the lipoxygenase inhibitor BWA4C in a dose-dependent manner. The most effective inhibition was exerted by BWA4C, suggesting metabolism of both PUFAs through the lipoxygenase pathway for growth stimulation. In vivo studies using the MAC26 tumour showed a significant stimulation of tumour growth when LA was administered orally at concentrations higher than 0.4 g kg-1 day-1. Higher concentrations did not produce a further increase in tumour growth rate. This suggests that there is a threshold dose for growth stimulation by LA which, together with that in the diet, amounted to 3.8% of the total caloric intake. The increase in tumour volume induced by LA arose from a reduction in the potential doubling time from 41 to 28 h and was effectively reversed by indomethacin (5 mg kg-1). These results suggest that PUFAs may play an important role in tumour growth and may offer a potential target for the development of chemotherapeutic agents.     

大鼠睾丸支持细胞培养方法在检测硫丹、己烯雌酚和氯化镉雄性生殖毒性中的应用

本研究在建立大鼠睾丸支持细胞体外培养方法的基础上, 观察了不同浓度的硫丹、氯化镉对睾丸支持细胞的毒作用, 发现它们对大鼠睾丸支持细胞均有毒作用, 且有良好的时间效应和剂量效应关系。另外还研究了皮下注射 20Λmol/kg 的氯化镉, 24h 后对所分离培养支持细胞存活的影响, 发现体内给予氯化镉后, 大鼠的支持细胞在体外培养4h 后存活率明显低于对照组 (P< 0. 05) 。随着培养时间的延长, 其存活率差距逐渐增大, 说明氯化镉可以透过血睾屏障到达支持细胞。本研究表明大鼠睾丸支持细胞体外测试系统具有快速、简便、终点明确、良好体内外一致性等优点, 可用于雄性生殖毒物的筛试和毒作用机理的评价。     

Malignancy-associated cellular markers (MAC) in oral and bronchial epithelial cells in sputum specimens: possible morphologic marker for high-risk groups (asbestos-exposed workers)

To verify a possible role of malignancy-associated cellular markers (MAC) in high-risk groups, the authors reviewed a total of 291 consecutive sputum specimens from 97 workers exposed to asbestos. The asbestos workers were matched according to smoking habits and cellular changes. Twelve subjects (12.3%) had MAC in epithelial cells; eight were smokers, four nonsmokers. Among MAC+ smokers, three sputum specimens contained cells of squamous metaplasia and one had cells from carcinoma in situ. Two MAC+ nonsmokers had cells of squamous metaplasia, too. In addition, MAC+ cells were also identified in four inflammatory samples, belonging either to smokers or nonsmokers. Two MAC+ subjects had a negative sputum specimen. In keeping with these results, the authors believe that MAC evaluation in sputum specimens might be of help in the oncologic follow-up of asbestos-exposed workers.     

C－myc癌基因在胃癌和癌前病变中的表达

 本研究采用生物素标记的C-myc癌基因为探针，检测70例胃部标本中C-myc癌基因mRNA的表达。结果发现C-myc癌基因的高表达在胃癌中占60.4%,在胃的良性病变中占27.27%,两者之间有显着性差异（P<0.05）.在48例胃癌的癌旁上皮中，C-myc癌基因高表达占37.5%,其中19例有不典型增生的癌旁上皮，高表达占78.95%,而无不典型增生的癌分上皮高表达只占10.34%.结果提示C-myc癌基因的高表达与胃粘膜上皮的异型增生有关，与胃癌的临床预后的关系还有待进一步探索。     

C－myc癌基因在胃癌和癌前病变中的表达

本研究采用生物素标记的Ｃ－ｍｙｃ癌基因为探针，检测７０例胃部标本中Ｃ－ｍｙｃ癌基因ｍＲＮＡ的表达。结果发现Ｃ－ｍｙｃ癌基因的高表达在胃癌中占６０．４％，在胃的良性病变中占２７．２７％，两者之间有显著性差异（Ｐ＜０．０５）。在４８例胃癌的癌旁上皮中，Ｃ－ｍｙｃ癌基因高表达占３７．５％，其中１９例有不典型增生的癌旁上皮，高表达占７８．９５％，而无不典型增生的癌分上皮高表达只占１０．３４％。结果提示Ｃ－ｍｙｃ癌基因的高表达与胃粘膜上皮的异型增生有关，与胃癌的临床预后的关系还有待进一步探索。     

Altered expression of Fhit in carcinoma and precarcinomatous lesions of the esophagus

The FHIT gene, located at chromosome 3p14.2, is a tumor suppressor gene often involved in tumors resulting from exposure to environmental carcinogens. We studied 46 pairs of esophageal primary tumors and corresponding normal squamous mucosa specimens by molecular genetic and immunohistochemical methods to investigate the role of the FHIT gene in esophageal carcinoma. In addition, we studied several different types of lesions, such as carcinoma in situ or dysplasia by immunohistochemistry. Loss of heterozygosity at or around the FHIT gene was observed in 35 (76%) primary tumors. Immunohistochemical detection of Fhit protein in the primary tumors demonstrated that 14 (30%) were positive and 32 (70%) were negative. We observed concordance between loss of Fhit protein and loss of heterozygosity and between loss of Fhit protein and RNA abnormalities. Because the FHIT/FRA3B locus is susceptible to damage by environmental carcinogens, we investigated the correlation between Fhit expression and smoking or alcohol habits. In this relatively small study, the patients who were both heavy users of tobacco and alcohol showed a significantly higher frequency of loss of Fhit expression than those who were light users. Noncarcinomatous squamous epithelium showed positive Fhit reactivity in most cases; however, five showed negative Fhit reactivity. Interestingly, all of these five patients had habits of heavy use of tobacco and alcohol. Eight of 12 carcinomas in situ, 2 of 4 severe dysplasias, 4 of 8 moderate dysplasias, and 3 of 9 mild dysplastic lesions showed negative Fhit reactivity. These findings indicated that loss of Fhit expression may be an early event in the development of human esophageal carcinoma and may occur even in normal-appearing squamous epithelium in some patients heavily exposed to environmental carcinogens.     

Urinary excretion of mutagens in smokers of cigarettes with various tar and nicotine yields, black tobacco, and cigars

Frameshift mutagens were isolated and concentrated from smokers' urine employing a method recently described. Urine concentrates of the habitual smokers and non-smokers who smoked cigarettes with low-, medium-, and high tar/nicotine yields, RCN (Reduced Condensate and Nicotine; artificial cigarettes containing cotobacco materials), black tobacco, and cigars were tested for mutagenicity in the Salmonella/mammalian microsome assay using Salmonella typhimurium TA98. Non-smokers who smoked 5 and habitual smokers who smoked 10 cigarettes of various tar and nicotine yields excreted more mutagens in urine with low-tar cigarettes than with medium- or high-tar cigarettes. Consuming more than 10 cigarettes a day resulted in a higher urinary excretion of mutagens with medium-tar cigarettes than with high-tar cigarettes. Smoking 5 RCN cigarettes a day by habitual smokers resulted in a higher urinary excretion of mutagens than smoking 5 commercial brand of cigarettes. In contrast, smoking 10 RCN cigarettes resulted in a lower urinary excretion of mutagens than smoking 10 commercial brand of cigarettes. The highest mutagenic activity was found with the urine of a habitual black tobacco smoker. Smoking cigars by non-smokers resulted in a very weak mutagenic activity of urine.