维生素C拮抗HgCl_2的致微核作用

研究表明,给小鼠腹腔注射HgCl_20.5和1.0mg/kg后,其诱发的微核率显著地高于蒸馏水对照组。而给小鼠腹腔注射VC50mg/kg以上,可降低HgCl_2的致微核作用,注射剂量达100和200mg/kg时,其作用更明显(P<0.001)。另外,不论是在HgCl_2染毒前4h或染毒后2h内给子VC,均可明显地降低HgCl_2的致微核作用,尤其是在HgCl_2染毒前30～60min内和染毒后30min时给VC、则其抗致微核作用愈益明显。如给小鼠饮用含VC2.5g/L的水一个月后,也可显著地降低HgCl_2的致微核作用。     

实验性苯中毒对骨髓红细胞微核改变的意义

目的 探讨苯的不同给药浓度对骨髓红细胞微核改变的影响,拟建立一种理想的苯中毒模型,为进一步苯的实验研究奠定基础.方法 昆明种小鼠50只,随机分为5组:1个对照组,4个实验组,每组10只.对照组单纯皮下注射生理盐水,实验组在每周一、三、五皮下注射苯制剂,并按所给苯剂量分为B1组(0.5 ml/kg体重)、B2组(1.0 ml/kg体重)、B3组(1.5 ml/kg体重)、B4组(2.0 ml/kg体重),各实验组分别于给苯前及给苯1、2.3、4周后称重动物,检测外周血及骨髓中红细胞微核的变化等指标.结果 ①与对照组相比,实验组小鼠白细胞、血红蛋白、血小板三项指标B1、B2组只部分指标改变,B3、B4组在给苯4周后全部指标与对照组相比差异有统计学意义(P均<0.05).②实验组小鼠外周血及骨髓红细胞微核率随着苯注射时间的延长呈现一定的上升趋势,在第3周出现高峰后,第4周下降.③第4周各实验组与对照组比较,小鼠骨髓嗜多染红细胞微核率明显上升,且差异有统计学意义(P均<0.05).结论 苯中毒可以导致小鼠外周血成熟红细胞和骨髓嗜多染红细胞微核率的增高,以此可作为检测骨髓红细胞受抑状态.     

苜蓿总皂苷的急性毒性和遗传毒性

背景与目的： 观察苜蓿总皂苷的急性毒性和遗传毒性。 材料与方法： 选择昆明种小鼠为受试对象,采用急性经口毒性试验测定苜蓿总皂苷的LD50;采用小鼠骨髓细胞微核试验、小鼠精子畸形试验对其遗传毒性进行评价。 结果： 苜蓿总皂苷的小鼠急性经口LD50为13.01 g/kg;95％可信限为12.46～13.58 g/kg。小鼠骨髓细胞微核和小鼠精子畸形试验结果均为阴性。 结论： 在本实验条件下,苜蓿总皂苷为实际无毒级;未发现遗传毒性。     

CB法微核图像中粘连淋巴细胞的自动分离

CB法微核图像中淋巴细胞的粘连情况可分为串联、并联、串并联三类。首先利用面积阈值、圆度阈值、延展度阈值提取串联的淋巴细胞区域;然后采用改进的基于凹点搜寻的分离方法对串联淋巴细胞区域进行分离,同时克服了崎岖边界的干扰问题;对于分离后的细胞,再判断其是否为双核淋巴细胞。这为CB法微核图像自动分析中串联淋巴细胞的判别和分离提供了一种切实可行的解决方法,有助于提高CB法微核图像分析的准确度和可靠性,而不影响自动分析的速度。     

汞、铅对小鼠睾丸和生殖细胞的亚慢性毒性

背景与目的: 研究重金属汞、铅对雄性小鼠睾丸和附睾精子的亚慢性毒性作用及其对生精细胞的遗传损伤。材料与方法:分别用高中低3种浓度氯化汞、醋酸铅经腹腔染毒4周龄雄性ICR小鼠,共10次,之后自由饲养23 d,于第50 d观察睾丸指数、附睾精子数量、精子活动率和精子头畸形率以及生精细胞微核率和减数分裂异常率。结果: 高浓度醋酸铅组小鼠睾丸指数低于对照组。中、高浓度氯化汞组、3种浓度醋酸铅组附睾精子密度低于对照组。中、高浓度醋酸铅组附睾精子活动率低于对照组。3种浓度氯化汞、醋酸铅致附睾精子畸形率升高。高浓度醋酸铅组生精细胞微核率高于对照组,3种浓度氯化汞和低、中浓度醋酸铅生精细胞微核率与对照组相比差异无显著性。各处理组减数分裂异常率与对照组差异均无显著性。 结论: 汞、铅暴露对小鼠精子具有亚慢性毒性作用,高浓度铅组影响生精细胞的微核率。     

白眉蝮蛇蛇毒精氨酸酯酶的致突变研究

目的与方法：采用Ames试验、小鼠骨髓嗜多染红细胞微核试验及小鼠精子畸形试验研究白眉蝮蛇(Agkistrodon halys ussuriensis )蛇毒中精氨酸酯酶有无致突变毒性,为临床应用提供安全性依据。结果与结论：3项试验均为阴性,精氨酸酯酶对所试菌株、小鼠体细胞及雄性生殖细胞均无诱变性。从致突变角度考虑,精氨酸酯酶在高于临床治疗剂量约100倍的条件下仍然安全。     

益母草对小鼠遗传物质损伤的影响

目的:观察中草药益母草对醋酸铅引起的小鼠遗传物质损伤的影响。方法：采用小鼠骨髓微核试验和小鼠精子畸形试验。结果：益母草本身不能诱发小鼠骨髓微核和小鼠精子畸形,但在与醋酸铅一同给药时,可使醋酸铅所诱发的小鼠骨髓微核和小鼠精子畸形频率明显降低。结论：益母草对小鼠遗传物质具有保护作用,即抗诱变作用。     

正常昆明种与NIH种小鼠自然发生微核率的比较

目的： 比较正常昆明种与NIH种小鼠胸骨骨髓嗜多染红细胞微核的自然发生率。 方法： 按《食品安全性毒理学评价程序和方法》采用30 h法微核试验,计数微核数,计算微核率。 结果： 小鼠胸骨骨髓PCE自然发生率呈正偏态分布,中位数能较好的代表其平均水平,昆明种小鼠胸骨骨髓PCE微核自然发生率(‰),雌鼠为1.0(0, 4.0),雄鼠为2.0(0, 6.0),性别间差异有统计学意义(P<0.05);NIH种小鼠胸骨骨髓PCE微核数自然发生率(‰),雌鼠为2.0(0, 3.0),雄鼠为2.0(0, 6.0),性别间差异无统计学意义。昆明种和NIH种小鼠胸骨骨髓PCE自发微核率间差异无统计学意义。 结论： 昆明种与NIH种小鼠胸骨骨髓PCE微核的自然发生率与其他人的研究较接近,昆明种与NIH种小鼠品系间差异无统计学意义,而昆明种小鼠性别间差异有统计学意义。     

Significance of formaldehyde-induced DNA–protein crosslinks for mutagenesis

Formaldehyde (FA) is a genotoxic substance, induces tumors in the nasal epithelium of rats, and is suspected to be a human carcinogen. As a primary DNA lesion, FA induces DNA–protein crosslinks (DPC) and the formation of DPC has been used as a measure of exposure for risk estimation. However, the significance of DPC for mutagenesis and carcinogenesis is at present poorly understood. We therefore performed comparative investigations on the induction of DPC and other genetic endpoints by FA in V79 Chinese hamster cells. The amount of DPC was comparatively determined with the K-SDS assay and the comet assay. Both tests gave similar results but the comet assay was much faster and easier to perform. Our results show that FA significantly induces DPC, sister-chromatid exchanges, and micronuclei in the same range of concentrations, parallel to the induction of cytotoxicity (relative cloning efficiency). In contrast, treatment of V79 cells with FA did not induce gene mutations in the HPRT test even after variations of the treatment protocol. Our results indicate that FA-induced DPC seem to be related to cytotoxicity and clastogenicity but do not lead to the formation of gene mutations in mammalian cells. It is suggested that FA-induced DPC do not cause gene mutations that are involved in FA-induced carcinogenesis. Environ. Mol. Mutagen. 32:260–268, 1998 © 1998 Wiley-Liss, Inc.     

1,4-Dioxane is not mutagenic in five in vitro assays and mouse peripheral blood micronucleus assay,but is in mouse liver micronucleus assay

1,4-Dioxane, an animal carcinogen, was not previously genotoxic in in vitro assays. We reevaluated the compound's genotoxic potential in five in vitro genotoxicity tests in the presence and absence of S9 mix using recommended new protocols. We used the bacterial reverse mutation assay with Salmonella TA and E. coli WP2 strains, including the plate and preincubation methods, the CHO chromosomal aberration assay, including examination of polyploid induction and extended sampling time, the CHO sister-chromatid exchange assay with short and long treatment time, the mouse lymphoma tk assay (microtiter method), including longer treatment time (24 hr), and the CHO micronucleus assay with short and long treatment times. The highest concentration we used was five mg/ml or plate. We also evaluated the genotoxic effect of 1,4-dioxane in vivo by conducting peripheral blood and liver micronucleus assays in the same mice after single oral administration of up to 3,000 mg/kg. All in vitro assays and the peripheral blood micronucleus assay were negative. The mouse liver micronucleus assay, on the other hand, was positive, indicating that 1,4-dioxane might be genotoxic. It is also conceivable that the positive result in mouse liver micronucleus assay was due to a nongenotoxic mechanism, i.e., errors in genetic repair following enhancement of hepatocyte proliferation. Environ. Mol. Mutagen. 32:269–280, 1998 © 1998 Wiley-Liss, Inc.