二溴乙腈对L5178Y细胞的遗传毒性及促凋亡作用

目的:研究饮用水中消毒副产物二溴乙腈对小鼠淋巴瘤L5178Y细胞的遗传毒性及促凋亡作用。方法:以L5178Y细胞为靶细胞,采用胞质分裂阻滞微核组学法(CBMN-cyt)和流式细胞术(FCM)分别检测不同浓度(0.1、1、5和10μmol/L)二溴乙腈对L5178Y细胞的遗传毒性及凋亡诱导作用。结果:与阴性对照比较,1和5μmol/L二溴乙腈染毒L5178Y细胞的微核率显著升高(P<0.05);1和10μmol/L二溴乙腈染毒L5178Y细胞的核质桥率显著升高(P<0.05);10μmol/L二溴乙腈染毒L5178Y细胞的核芽率升高(P<0.05);5和10μmol/L二溴乙腈染毒L5178Y细胞的核分裂指数率显著下降(P<0.05)。二溴乙腈各剂量组L5178Y细胞凋亡率均明显高于对照组,差异均具有统计学意义(P均<0.05)。结论:二溴乙腈可致L5178Y细胞遗传毒性并诱导其凋亡。     

纳米银对人肺癌和肝癌细胞毒性的差异

目的:研究纳米银对人肺癌(A549)和人肝癌(HepG2)细胞系增殖和凋亡的影响,并探讨纳米银对两种细胞系毒效应的差异及其机制。方法:用20、40、80、160、320、640 μg/mL的纳米银分别染毒A549和HepG2细胞,染毒时长均为24和48 h,以细胞培养液为对照,采用MTT法检测各组细胞的存活率;谷胱甘肽(GSH)和超氧化物歧化酶(SOD)试剂盒检测细胞内GSH含量和SOD活力。除上述各染毒组,两种细胞均另设置N-乙酰半胱氨酸(NAC)预处理后160 μg/mL纳米银染毒组,采用流式细胞术检测各组细胞凋亡率。结果:与对照组比较,染毒24和48 h后, ≥40 μg/mL剂量组A549细胞和所有剂量组HepG2细胞存活率均降低(P<0.05或P<0.01);与相同染毒条件下的A549细胞比较,40~640 μg/mL剂量组HepG2细胞的存活率较高(P<0.05或P<0.01)。SOD活力和GSH含量检测发现,纳米银染毒A549细胞24 h后,40 μg/mL剂量组SOD活力与对照组比较显著降低(P<0.05),而GSH含量上升(P<0.05);染毒48 h后,SOD活力和GSH含量在40~160 μg/mL剂量组下降,其中80 μg/mL剂量组GSH含量与对照组间的差异显著(P<0.05)。纳米银染毒HepG2细胞24、48 h后,SOD活力和GSH含量都表现为上升,其中40、80 μg/mL组SOD活力和20 μg/mL组GSH含量与对照组间的差异显著(P<0.05)。细胞凋亡率检测发现,染毒24 h时,各剂量组A549细胞凋亡率与对照组比较差异无统计学意义(P>0.05),而各剂量组HepG2细胞凋亡率均显著增加(P<0.05或P<0.01);染毒48 h时, ≥40 μg/mL剂量组A549细胞和160 μg/mL剂量组HepG2细胞凋亡率均高于对照组(P<0.05或P<0.01)。使用NAC预处理细胞后,160 μg/mL剂量组两种细胞系凋亡率均显著下降(P<0.01)。结论:纳米银可以引起A549和HepG2细胞表现不同程度的增殖抑制和凋亡,而细胞内不同的SOD和GSH改变可能是纳米银引起两种细胞系不同毒作用的原因之一。     

活性氧在异烟肼诱导L-02细胞DNA损伤中的作用及槲皮素的保护效应

目的：探讨活性氧（ROS）在异烟肼（INH）诱导的L-02细胞DNA损伤中的作用及槲皮素的保护效应。方法：将L-02细胞分为空白对照组、INH组（10 mmol/L INH）;槲皮素低剂量组（10 mmol/L INH+25 μmol/L槲皮素）;槲皮素高剂量组（10 mmol/L INH+50 μmol/L槲皮素）。细胞处理24 h后,采用彗星试验检测细胞DNA损伤情况;分别应用荧光探针DCFH-DA和Rhodamine123检测细胞ROS水平及线粒体膜电位。结果：与空白对照组比较,L-02细胞经INH和槲皮素处理后,INH组细胞尾部DNA百分含量、尾长和尾矩均显著增加（P<0.01）;与INH组相比,低和高剂量槲皮素组细胞的尾部DNA百分含量、尾长和尾矩均明显减少（P<0.05或P<0.01）。INH组细胞线粒体ROS水平比空白对照组显著升高（P<0.01）;而低和高剂量槲皮素组细胞线粒体ROS水平比INH组明显降低（P<0.05或P<0.01）。INH组细胞线粒体膜电位显著低于空白对照组（P<0.01）,而低和高剂量槲皮素组细胞线粒体膜电位明显高于INH组（P<0.05或P<0.01）。结论：INH能诱导L-02细胞DNA损伤,ROS介导的线粒体损伤在INH诱导L-02细胞DNA损伤的过程中发挥了重要作用;槲皮素对INH诱导L-02细胞DNA损伤具有保护效应,可能与其抑制ROS介导的线粒体损伤有关。     

采用体内碱性彗星试验检测两种聚醚醚酮材料的遗传毒性

目的：采用哺乳动物体内碱性彗星试验,检测两种聚醚醚酮材料的遗传毒性,为医疗器械及其材料的遗传毒性体内碱性彗星试验方法的建立提供依据。方法：采用0.9%氯化钠注射液(SC)和棉籽油(CSO)两种介质制备聚醚醚酮材料的试验液,以SC和CSO作为阴性对照,甲基磺酸甲酯(MMS)作为阳性对照。选取 SD大鼠 70只,雌雄各半,大鼠连续两次(间隔 24 h)染毒,SC组和MMS阳性对照组按照 10 mL/kg的剂量由静脉途径染毒,CSO组按照 5 mL/kg的剂量由腹腔途径染毒,末次染毒后 3 h处死大鼠,称取肝脏和肾脏的质量并进行组织病理学检查。取肝脏、肾脏和外周血分别制备单细胞悬液进行碱性彗星试验,以尾部DNA百分比、尾矩和Olive尾矩为分析指标判断DNA损伤程度。结果：试验组的大鼠肝脏系数、肾脏系数分别与SC和CSO阴性对照组相比差异均无统计学意义(P >0.05),所有大鼠的肝脏和肾脏形态结构正常,未见明显的组织病理学改变。与 SC和 CSO阴性对照组相比,MMS阳性对照组尾部DNA含量百分比、尾矩和Olive尾矩的差异有统计学意义(P<0.01),两种聚醚醚酮材料组间的差异无统计学意义(P>0.05)。结论：应用体内碱性彗星试验的研究方法,在本研究条件下,两种聚醚醚酮材料的试验液不能诱导大鼠肝细胞DNA链断裂,未检测出遗传毒性。     

甲醛对HepG2细胞游离胆固醇代谢的影响

目的：研究甲醛（FA）对人肝癌细胞株HepG2细胞游离胆固醇（FC）含量的影响及其作用机制。方法：分别采用0.004、0.02、0.1 mmol/L FA处理人肝癌细胞株HepG2细胞24和48 h,以完全培养基为阴性对照,过氧化物酶法测定HepG2细胞内FC含量;采用Western blot法检测HepG2细胞固醇调节元件结合蛋白-2（SREBP-2）、羟甲基戊二酸单酰辅酶A还原酶（HMGCR）、胆固醇酰基转移酶（ACAT）和低密度脂蛋白受体（LDLR）的蛋白表达水平。结果：与阴性对照组相比,各浓度的FA染毒24 h或0.02和0.1 mmol/L FA染毒48 h后,HepG2细胞内FC含量均明显增加（P均 < 0.05）;FA染毒24和48 h后细胞内HMGCR蛋白表达水平均明显增加（P < 0.05）;FA染毒24 h后,ACAT和LDLR表达水平均明显降低（P均 < 0.05）;FA染毒48 h,LDLR蛋白表达水平明显降低（P < 0.05）,ACAT蛋白表达水平在0.02和0.1 mmol/L FA组明显降低（P < 0.05）。结论：甲醛染毒可使HepG2细胞内FC含量增加,可能与胆固醇的从头合成增加和胆固醇酯化水平降低有关。     

汞、砷、甲醛单一及复合污染对蚕豆根尖细胞微核的影响及污染评价

目的：探讨水环境中汞、砷、甲醛及其复合污染对蚕豆根尖细胞微核的影响及污染评价。方法：以蒸馏水作为阴性对照组,50 mg/L重铬酸钾作为阳性对照组,使用不同浓度的汞（0.001~0.03 mg/L）、砷（0.01~0.3 mg/L）、甲醛（0.9~7.2 mg/L）及其组合对蚕豆进行染毒（设MIX I、MIX Ⅱ、MIX Ⅲ3组,各含4种组合）,测定蚕豆根尖细胞的微核千分率并计算污染指数。结果：单一染毒时,当水溶液中汞浓度≥0.009 mg/L、砷浓度≥0.3 mg/L、甲醛浓度≥3.6 mg/L时蚕豆根尖细胞微核千分率均高于阴性对照组,且差异均具有统计学意义（P<0.05）。复合污染中,MIX I组砷-汞、砷-甲醛组合蚕豆根尖细胞微核千分率与阴性对照组相比显著升高,而且较砷、汞、甲醛单一染毒时明显增加,差异均具有统计学意义（P<0.05）。MIX Ⅱ组和MIX Ⅲ组中4种组合的蚕豆根尖细胞微核千分率与阴性对照组相比均显著升高,并且均明显高于单一染毒时的微核千分率,差异均具有统计学意义（P<0.05）。结论：汞（≥0.009 mg/L）、砷（≥0.3 mg/L）、甲醛（≥3.6 mg/L）可诱导蚕豆根尖细胞形成微核,复合染毒诱发的微核千分率较相同剂量单一溶液染毒呈不同程度的升高,并且存在一定的量效关系。     

纳豆脂肽诱导人乳腺癌细胞MCF-7凋亡的机制研究

目的:初步探讨纳豆脂肽诱导人乳腺癌细胞MCF-7凋亡的可能作用机制。方法:取对数生长期的MCF-7细胞,实验设4组,分别加入不同浓度(0、1、2、4μg/mL)的纳豆脂肽,于37℃培养箱中继续培养12 h后,收集细胞,采用流式细胞术检测纳豆脂肽对MCF-7细胞凋亡的影响;单细胞凝胶电泳检测纳豆脂肽对MCF-7细胞DNA损伤的影响;Western blot法检测纳豆脂肽对雌激素受体ERα和ERβ蛋白表达的影响。结果:与对照组比较,各浓度纳豆脂肽处理组均可诱导MCF-7细胞凋亡(P均<0.05);Olive尾矩和尾部DNA含量均明显增加(P<0.05或P<0.01),且4μg/mL纳豆脂肽组尾长亦明显增加(P<0.01)。纳豆脂肽浓度为4μg/mL时,ERα表达水平明显下降,ERβ表达水平明显上升,差异均具有统计学意义(P均<0.05)。结论:纳豆脂肽可能是通过影响MCF-7细胞内雌激素受体表达水平和引起DNA损伤来诱导MCF-7细胞发生凋亡。     

苯并(a)芘染毒致人支气管上皮细胞的周期改变及BPDE-DNA加合物形成

目的:通过观察苯并(a)芘(BaP)染毒致人支气管上皮细胞16HBE细胞周期改变及BPDE-DNA加合物形成的情况,探讨DNA损伤与细胞周期阻滞之间的关系。方法:用不同浓度BaP(0、1、2、4、8、16、32 μmol/L)染毒16HBE细胞24 h,用16 μmol/L BaP染毒16HBE细胞不同时间(0、1、2、4、8、12、24 h)以检测BaP染毒16HBE细胞的剂量和时间效应。再根据上述结果选择16 μmol/L BaP染毒16HBE细胞4 h后,恢复不同时间(0、1、2、4、8、12、24 h),处理结束后采用流式细胞术检测细胞周期分布情况,酶联免疫法和荧光免疫组化法检测BPDE-DNA加合物表达。结果:与正常对照组相比,随着BaP染毒浓度和染毒时间的增加,S期细胞所占比例均增加(P<0.05或P<0.01)。16 μmol/L BaP染毒16HBE细胞4 h后,恢复早期(4~12 h)S期细胞所占比例与恢复0 h相比明显增加(P<0.05),恢复24 h时S期细胞所占比例(24.52%)与恢复0 h相比明显降低(P<0.01),而与正常对照组(26.41%)相比差异无统计学意义(P>0.05)。随着染毒浓度增加和染毒时间延长,16HBE细胞内BPDE-DNA加合物含量逐渐增加,与正常对照组相比差异均有统计学意义(P<0.01),染毒后恢复1 h时BPDE-DNA加合物含量与恢复0 h组相比显著增加(P<0.01),而后随恢复时间延长逐渐下降。回归分析显示BaP染毒后细胞S期所占比例与BPDE-DNA加合物含量符合Cubic方程(R²=0.386,P=0.01)。结论:BaP染毒所致BPDE-DNA加合物的形成与S期阻滞密切相关。     

G6PD缺陷对 1,4-苯醌致K562细胞DNA甲基化的影响及其机制

目的：研究G6PD缺陷对1,4-苯醌（1,4-BQ）致K562细胞DNA甲基化的影响及其机制。方法：分别采用10和20 μmol/L的1,4-BQ溶液对G6PD缺陷K562细胞和正常表达细胞进行染毒,以未染毒组为对照,各组均设置12、24、48 h共3个染毒时间,另在20 μmol/L 1,4-BQ染毒组细胞中加入1.5 mmol/L谷胱甘肽（GSH）进行干预。采用比色法检测全基因组DNA甲基化相对水平,qPCR法检测甲基转移酶DNMT1、DNMT3a、DNMT3b mRNA表达水平,Western blot法检测DNMT1、DNMT3a蛋白表达水平。结果：10和20 μmol/L 1,4-BQ染毒后的K562细胞全基因组DNA甲基化水平升高（P<0.05）,除20 μmol/L 1,4-BQ染毒48 h组外,其他各染毒组的G6PD缺陷K562细胞全基因组DNA甲基化水平均高于正常细胞（P<0.05）。在1,4-BQ染毒后,G6PD缺陷细胞的DNMT1、DNMT3a、DNMT3b mRNA水平以及DNMT1、DNMT3a蛋白表达水平均高于正常细胞（P<0.05）。加入GSH后,G6PD缺陷细胞和正常细胞的全基因组DNA甲基化相对水平、DNMTs mRNA及蛋白表达水平的差异的无统计学意义（P均>0.05）。结论：G6PD缺陷可能以抑制K562细胞GSH合成的方式增加氧化应激水平,最终导致细胞DNMTs生成的增多以及全基因组DNA甲基化程度的升高。     

年龄和性别对正常人外周血淋巴细胞核质桥自发率的影响

目的： 探索年龄、性别因素对我国健康人群外周血淋巴细胞核质桥自发率的影响,为核质桥的影响因素研究提供科学依据。方法： 选取98例健康成人,其中男性52例,女性46例,年龄范围为20~68岁,平均年龄为（40.7±12.6）岁。按年龄分为20~29岁组（22人）、30~39岁组（23人）、40~49岁组（25人）和50岁以上组（28人）。抽取研究对象外周血2 mL,采用胞质分裂阻滞法培养细胞40 h后,加入松胞素B （终浓度为10 μg/mL）,继续培养至68 h收获细胞。每个受试者观察1 000个双核细胞,分析核质桥、微核及核芽的数量。结果： 核质桥总体自发率为每个细胞0.56‰,男性略高于女性,但差异无统计学意义（P > 0.05）。男性在不同年龄组间,核质桥自发率差异无统计学意义（P > 0.05）。女性40~49岁年龄组核质桥自发率最高,显著高于20~29岁组（U=2.31,P < 0.05）。微核自发率女性高于男性（U=4.40,P < 0.05）,男性和女性受试者40~49岁组微核自发率均为最高。核芽自发率在不同性别间的差异无统计学意义（P > 0.05）,在不同年龄组间无明显变化规律。结论： 健康人群中的核质桥自发率较低,不受性别因素影响,在20~49岁范围内具有随年龄增加而升高的趋势。     

Cytokinesis-blocked micronucleus assay as a novel biomarker for lung cancer risk

In this case-control study, we modified the cytokinesis-block micronucleus (CBMN) assay, an established biomarker for genomic instability, to evaluate susceptibility to the nicotine-derived nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) by measuring the frequency of NNK-induced chromosomal damage endpoints (micronuclei, nucleoplasmic bridges, and nuclear buds) per 1,000 binucleated lymphocytes. Spontaneous and NNK-induced chromosomal damage were significantly higher in lung cancer patients compared with controls. Forty-seven percent of cases (versus 12% of controls) had >or=4 spontaneous micronuclei, 66% of cases (and no controls) had >or=4 spontaneous nucleoplasmic bridges, and 25% of cases (versus 5% of controls) had >or=1 spontaneous nuclear bud (P < 0.001). Similarly, 40% of cases (versus 6% of the controls) had >or=5 NNK-induced micronuclei, 89% of cases (and no controls) had >or=6 induced nucleoplasmic bridges, and 23% of cases (versus 2% of controls) had >or=2 induced nuclear buds (P < 0.001). When analyzed on a continuous scale, spontaneous micronuclei, nucleoplasmic bridges, and nuclear buds were associated with 2-, 29-, and 6-fold increases in cancer risk, respectively. Similarly, NNK-induced risks were 2.3-, 45.5-, and 10-fold, respectively. We evaluated the use of CBMN assay to predict cancer risk based on the numbers of micronuclei, nucleoplasmic bridges, and nuclear buds defined by percentile cut points in controls. Probabilities of being a cancer patient were 96%, 98%, and 100% when using the 95th percentiles of spontaneous and NNK-induced micronuclei, nucleoplasmic bridges, and nuclear buds, respectively. Our study indicates that the CBMN assay is extremely sensitive to NNK-induced genetic damage and may serve as a strong predictor of lung cancer risk.     

乙二胺为核心的PAMAM树枝状聚合物(5.0代)纳米材料溶液的遗传毒性研究

目的:研究乙二胺为核心的PAMAM树枝状聚合物(5.0代)纳米材料溶液的遗传毒性。方法:采用Ames试验平板掺入法,设3 985、797、139.4、31.88和6.376 μg/皿的5个乙二胺为核心的PAMAM树枝状聚合物(5.0代)溶液浓度组,在加与不加S9混合液的条件下观察回变菌落数。同时采用L5178Y细胞胞质分裂阻滞微核细胞组学试验,给予受试细胞终浓度分别为0.625、1.25、2.5、5、10 μg/mL的受试物,观察其微核组效应、剂量-效应和时间-效应关系。结果:受试物溶液各剂量组均未引起测试菌株回变菌落数明显增加,Ames试验结果为阴性。胞质分裂阻滞微核细胞组学试验中,与阴性对照组比较,1.25 μg/mL的受试物即可诱导受试细胞出现核芽(P<0.01);2.5 μg/mL及以上剂量可进一步诱使细胞出现总微核、Ⅰ型微核、Ⅱ型微核和核质桥效应(P<0.01),且存在明显的剂量-效应关系(除核质桥外,r值均>0.5,P均<0.05)。与阴性对照组比较,在5 μg/mL剂量下,乙二胺为核心的PAMAM树枝状聚合物(5.0代)溶液在9 h时即可诱导受试细胞的总微核、Ⅰ型微核、Ⅱ型微核和核芽增加(P<0.01);在18 h时出现核质桥数增加(P<0.01),各项指标在27 h达到峰值。结论:乙二胺为核心的PAMAM树枝状聚合物(5.0代)溶液对鼠伤寒沙门氏菌无致基因突变作用;对L5178Y细胞可诱导4类微核组效应,并有明显的剂量-效应和时间-效应关系;从剂量和时间来看,以核芽效应最为敏感。     

Cytokinesis-blocked micronucleus cytome assay biomarkers identify lung cancer cases amongst smokers.

The multi-endpoint cytokinesis-blocked micronucleus assay is used for assessing chromosome aberrations. We have recently reported that this assay is extremely sensitive to genetic damage caused by the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and that the binucleated cells with micronuclei, nucleoplasmic bridges, and nuclear buds in lymphocytes (chromosome damage endpoints measured by the assay) are strong predictors of lung cancer risk. In the current study, we refined our analysis to include toxicity endpoints (micronuclei in mononucleated cells, apoptosis, necrosis, and nuclear division index) to investigate the benefit of including these variables on improving the predictive value of the assay. Baseline and NNK-induced micronuclei in mononucleated cells were significantly higher in patients (n = 139) than controls (n = 130; P < 0.001). Baseline apoptosis was higher among cases; however, the controls showed a significant higher fold increase in NNK-induced apoptosis compared with baseline (P < 0.001). Principal components analysis was used to derive a summary measure for all endpoints and calculate the positive predictive value (PPV) and negative predictive value (NPV) for disease status. First principal component for NNK-induced chromosome damage endpoints (binucleated cells with micronuclei, nucleoplasmic bridges, and nuclear buds) had an area under the curve = 97.9 (95% confidence interval, 95.9-99.0), PPV = 94.8, and NPV = 92.6. The discriminatory power improved when micronuclei in mononucleated cells were included: area under the curve = 99.1 (95% confidence interval, 97.9-100.0), PPV = 98.7 and NPV = 95.6. The simplicity, rapidity, and sensitivity of the assay together with potential for automation make it a valuable tool for screening and prioritizing potential cases for intensive screening.     

No acute and persistent DNA damage after an Ironman triathlon

During acute and strenuous exercise, the enhanced formation of reactive oxygen species can induce damage to lipids, proteins, and nucleic acids. The aim of this study was to investigate the effect of an Ironman triathlon (3.8 km swim, 180 km cycle, 42 km run), as a prototype of ultra-endurance exercise, on DNA stability. As biomarkers of genomic instability, the number of micronuclei, nucleoplasmic bridges, and nuclear buds were measured within the cytokinesis-block micronucleus cytome assay in once-divided peripheral lymphocytes of 20 male triathletes. Blood samples were taken 2 days before, within 20 min after the race, and 5 and 19 days post-race. Overall, the number of micronuclei decreased (P < 0.05) after the race, remained at a low level until 5 days post-race, and declined further to 19 days post-race (P < 0.01). The frequency of nucleoplasmic bridges and nuclear buds did not change immediately after the triathlon. The number of nucleoplasmic bridge declined from 2 days pre-race to 19 days post-exercise (P < 0.05). The frequency of nuclear buds increased after the triathlon, peaking 5 days post-race (P < 0.01) and decreased to basic levels 19 days after the race (P < 0.01). The results suggest that an Ironman triathlon does not cause long-lasting DNA damage in well-trained athletes.     

In vivo genotoxicity of hard metal dust: induction of micronuclei in rat type II epithelial lung cells

Inhalation of hard metal dust (WC-Co particles) has been associated with an increased risk for lung cancer in occupational settings. In vitro, WC-Co was genotoxic in human lymphocytes producing DNA strand breaks and micronuclei. The aim of the present study was to evaluate the in vivo genotoxic effects of WC-Co dust in rat type II pneumocytes. DNA breaks/alkali-labile sites (alkaline comet assay) and chromosome/genome mutations (micronucleus test) were assessed after a single intra-tracheal (i.t.) instillation of WC-Co, including dose-effect and time trend relationships. In addition, the alkaline comet assay was performed on cells obtained after broncho-alveolar lavage (BAL) and on peripheral blood mononucleated cells (PBMC). As pulmonary toxicity parameters, protein content, lactate dehydrogenase activity, total and differential cell count in BAL fluid were evaluated in parallel. In type II pneumocytes, WC-Co induced a statistically significant increase in tail DNA (12 h time point) and in micronuclei (72 h) after a single treatment with 16.6 mg WC-Co/kg body wt, a dose that produced mild pulmonary toxicity. This observation provides the first evidence of the in vivo mutagenic potential of hard metal dust. In PBMC, no increase in DNA damage or micronuclei was observed. This study indicates the potential to detect chromosome/genome mutations (micronuclei) in relevant target cells (type II pneumocytes) after i.t. instillation of a particle mixture.     

Polyphenol Content,Antioxidant, Cytotoxic,and Genotoxic Activities of Bombax ceiba Flowers in Liver Cancer Cells Huh7

Objective: Bombax ceiba (red Silk cotton tree) has great ethnopharmacological significance due to its widespread use to treat various diseases such as dysentery, inflammation, and tuberculosis. Despite decades of research, the studies on the in vitro anticancer/genotoxic activity of B. ceiba flower remains restricted. Thus, the present research explored the effect of ethanol extract from B. ceiba flowers on three human cancer cells, including lung A549 and liver HepG2 and Huh7 cell lines. Methods: Cytotoxic and genotoxic activity of B. ceiba extract was examined by MTT and comet assay, respectively. Further, B. ceiba extract was analysed to determine total polyphenol content and DPPH antiradical scavenging activity. Results: ethanol extract from B. ceiba flowers had a high polyphenols content with very potent antioxidant activity. Further, B. ceiba extract displayed moderate cytotoxicity against Huh7 cells and no cytotoxicity against HepG2 and A549 cells. The comet assay findings showed that Huh7 cells treated with four concentrations of B. ceiba extract (¼ IC50, ½ IC50, IC50, and double IC50) increased the comet tail formation within 48 h in a concentration-dependent manner. Conclusion: ethanol extract from B. ceiba flowers exhibited its cytotoxicity through induction of DNA fragmentation in Huh7 cells.     

铅暴露工人外周血淋巴细胞遗传损伤与端粒长度的改变

目的:探讨铅暴露工人外周血淋巴细胞遗传损伤情况与端粒长度改变之间的关系。方法:以珠三角某蓄电池厂的21名铅暴露工人为铅暴露组,26名无铅接触史的工人作为对照组。针对工人开展问卷调查并采集肝素抗凝外周血。检测工人外周血中血铅浓度、淋巴细胞的彗星试验指标、胞质分裂阻滞微核试验指标以及相对端粒长度改变情况。结果:铅暴露工人的血铅浓度为(3.08±1.86) mg/mL,与对照人群(0.26±0.25) mg/mL相比明显升高(P<0.05)。彗星试验中,铅暴露组工人的慧星尾长高于对照组(P<0.05);胞质分裂阻滞微核试验中,暴露组工人双核微核率和微核细胞率均高于对照组(P<0.05);铅暴露工人的外周血相对端粒长度较对照人群缩短(P<0.05)。相关分析结果显示,胞质阻滞微核试验的指标中双核微核率、微核细胞率、核桥率与工龄呈正相关(r_s分别为0.447、0.432、0.351,P均<0.05)。外周血相对端粒长度与工人工龄、血铅水平均呈负相关(r_s分别为-0.306、-0.394,P均<0.05)。结论:铅暴露可致工人外周血淋巴细胞的遗传损伤以及相对端粒长度的缩短。     

叶酸对乙醇诱发的人成淋巴细胞遗传损伤的影响

目的：探讨叶酸（folic acid,FA）对乙醇（ethanol,EtOH）诱发的人成淋巴细胞遗传损伤的影响。方法：人成淋巴细胞株GM12593培养在含有不同FA浓度（20、200、2000 nmol/L）的RPMI-1640培养基中,并同时在每种FA浓度的培养体系中分别加入0.09%、0.36%和1.34%（V/V）的EtOH,8 d后用细胞松弛素B（cytochalasin B,CB）处理28 h,胞质阻断微核细胞组分析（cytokinesisblockmicronucleus cytome assay,CBMN Cyt）比较不同培养条件下的细胞遗传损伤,包括微核化双核细胞（micronucleated binucleatedcell,MNed BNC）、核芽（nuclear bud,BUD）、核质桥（nucleoplasmic bridges,NPB）的频率差异。结果：乙醇在受试细胞中诱发MNedBNC、BUD和NBP频率显著升高（P〈0.01）;2 000 nmol/L的叶酸能显著降低由乙醇诱发的MNed BNC、BUD和NBP频率（P〈0.01）。结论：乙醇对细胞遗传物质具有损伤效应,叶酸对乙醇的遗传毒性具有防护效应。     

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.