As2O3处理前后K562细胞基因表达变化的基因芯片检测

目的应用基因芯片研究三氧化二砷(As2O3)处理前后K562细胞基因表达的变化.方法提取As2O3处理前后K562细胞的总RNA,纯化为mRNA后再反转录为cDNA.cDNA经限制性内切酶Sau3AI切割后,cDNA片段分别用Cy3和Cy5标记,与自制的包含348个基因片段的胎盘库芯片杂交.结果杂交结果经扫描和软件分析,发现了11个差异表达的基因片段,其中有3个基因片段与细胞凋亡密切相关.结论我们构建的胎盘库基因芯片可以成功地用于研究药物作用前后基因表达的变化.     

谷胱甘肽、自由基在砷剂诱导卵巢癌细胞凋亡中的作用

目的　观察谷胱甘肽、自由基在砷剂诱导卵巢癌细胞凋亡中的作用。方法　砷剂孵育卵巢癌细胞 4 8h后 ,琼脂糖凝胶电泳及流式细胞仪检测细胞凋亡 ,分光光度法检测细胞内谷胱甘肽、活性氧及丙二醛含量。结果　砷剂具有诱导卵巢癌细胞凋亡作用 ,砷剂诱导后细胞内谷胱甘肽含量减少 (P <0 .0 1)、活性氧及丙二醛含量增加(P <0 .0 5 )。结论　氧化还原系统的改变是砷剂诱导卵巢癌细胞凋亡的重要途径之一。     

不同浓度三氧化二砷对哮喘小鼠气道树突状细胞的作用

目的 :研究 3种不同浓度三氧化二砷 (arsenictrioxide,As2 O3)对哮喘小鼠气道树突状细胞 (dendriticcells ,DCs)分布和募集的作用。方法 :BALB c小鼠 5 0只随机分为5组 ,即对照组、哮喘组、低剂量 (1mg kg)As2 O3组、中剂量 (5mg kg)As2 O3组和高剂量 (10mg kg)As2 O3组。采用免疫组织化学染色、计算机图像分析和扫描电镜技术分别检测气道DCs。结果 :对照组小鼠整个肺组织构成了一个NLDC 14 5 +DCs网络 ,NLDC 14 5 + DCs密度从大气道到小气道分别为(5 0 0± 5 0 )个 mm2 到 (6 0± 10 )个 mm2 上皮面积 (P <0 0 5 ) ;哮喘组小鼠肺内NLDC 14 5 + DCs密度较对照组显著增加 (P <0 .0 1) ,但不影响其肺内分布 ;哮喘小鼠经As2 O3处理后 ,肺内NLDC 14 5 + DCs密度显著下降 (P <0 0 1) ,但不影响其肺内分布 ,且三种不同浓度砷剂处理组间无显著性差异 (P >0 0 5 )。结论 :下调肺内DCs密度而不影响其肺内分布 ,可能是As2 O3治疗哮喘的一个重要机制 ;低剂量As2 O3治疗哮喘具有潜在的应用前景。     

As_2O_3诱导人肝癌细胞凋亡及对Fas表达和钙含量的影响

化疗在原发性肝癌的综合治疗中占重要地位.为寻找肝癌治疗新的有效药物,我们观察了As2O3对人肝癌细胞株BEL7402的生物学效应,以期为As2O3临床治疗肝癌提供实验依据.     

Arsenical necrosis of the jaws

After a brief historical review of the use of arsenic in dental practice two cases of arsenical necrosis of the jaws, affecting the maxilla and mandible respectively, are reported. Both patients were treated conservatively over an extended period with excellent results. It is concluded that there is no justification, whatsoever, for the use of arsenic in modern dental practice and that, although prolonged, conservative treatment of chemical necrosis of the jaws is preferable to more radical treatment.     

Assessment of exposure to arsenic among smelter workers: A five-year follow-up

In a group of 43 smelter workers exposed to inorganic arsenic dust for 13-45 years, nerve conduction velocities (NCVs) were significantly lower in two peripheral nerves as compared with matching referents. With multivariate data analysis, a significant negative correlation was found between cumulative absorption of arsenic and NCV in four examined nerves and the sural amplitude. Clinical symptoms of neuropathy and other symptoms related to arsenic exposure were moderate, though the difference between the groups was significant. The mean total absorption of arsenic was calculated to be less than 5 g, and the maximal absorption about 20 g. These data indicate that the adverse effect of arsenic on the peripheral nerves is dependent on long-term exposure rather than on short-term fluctuations in exposure levels. © 1994 Wiley-Liss, Inc.     

口服二巯基丁二酸治疗狗路易氏剂中毒

为证实口服二巯基丁二酸（ＤＭＳＡ）治疗路易氏剂中毒的效价，以狗为实验动物，进行实验治疗研究，狗口服ＤＭＳＡ（４０～１２０ｍｇ／ｋｇ）后，２周内未见到有关的生理，生化指标明显变化，该药毒性较小。ＤＭＳＡ可在肠道内较好地被吸收，与静脉注射途径比较，口服组血药浓度上升慢，下降亦慢，可在体内维持较长时间，ＤＭＳＡ在体内促排砷的作用与静脉注射同剂量ＤＭＳＡ（钠盐）相当。狗口服ＤＭＳＡ４０ｍｇ／ｋｇ可对抗路易     

三氧化二砷诱导慢性髓系白血病细胞G2/M周期停滞及其机理

目的 研究三氧化二砷对慢性髓系白血病细胞的体外作用特点及其机理。方法 将三氧化二砷与慢性髓性白血病细胞系K562作用后，测定细胞的生长曲线及活性，流式细胞测量术检测细胞凋亡和细胞周期分布的改变；同时，采用RT-PCR方法检测药物作用前后细胞周期相关基因表达的变化。结果 ①三氧化二砷明显抑制K562细胞的生长，其作用呈时间和浓度依赖性；②三氧化二砷诱导K562细胞凋亡的作用较弱，但可明显诱导K562细胞在G2／M期停滞，此效应也呈时间和浓度依赖性；③三氧化二砷作用后，细胞周期抑制基因p57表达明显上调，而细胞周期促进基因cyclinB的表达受到抑制。结论 三氧化二砷能有效抑制慢性髓系白血病细胞的生长，其机理主要为诱导细胞G2／M期周期停滞；该效应与细胞周期相关基因的表达变化有关。     

Arsenic trioxide exposure to ovarian carcinoma cells leads to decreased level of topoisomerase II and cytotoxicity

The objective of this study was to investigate the effect of arsenic trioxide (As(2)O(3)) on topoisomerase II levels using western blotting method on MDAH 2774 ovarian carcinoma cell culture. Experimental designs were established to determine the cytotoxic effects of As(2)O(3) on MDAH 2774 cells and the IC50 (fatal dose for the 50% of cells) value. Cytotoxicity experiments were carried out using various concentrations of As(2)O(3). The 2,3-bis[2-methyloxy-4-nitro-5-sulfophenyl]-2H-tetrazolium-5-carboxanilide (XTT) and trypan blue dye-exclusion tests were used to evaluate cytotoxicity. Topoisomerase II expressions were investigated using western blotting method with various concentrations of As(2)O(3). Densitometric analysis of topoisomerase 2 bands was carried out using Quantity One 1-D analysis software (Bio-Rad USA, Life Science Research, Hercules, CA). IC50 value of As(2)O(3) was found to be 5 x 10(-6) M for MDAH 2774 cells. When the bands were evaluated, it was observed that there was a decrease in topoisomerase II levels in MDAH 2774 cells with increasing concentrations of As(2)O(3). It was also observed by the densitometric analysis that topoisomerase II expression ratios of MDAH 2774 cells were decreased by approximately 50% at this concentration. Topoisomerase II levels were significantly decreased with the increasing concentrations of As(2)O(3). Inhibition of topoisomerase II enzyme was one of the antiproliferative influence mechanisms of As(2)O(3).