有机砷锑药物中砷锑之含量测定

有机砷锑化合物中砷锑的测定在药品鉴定及有机化合物的分析研究上均有很大的价值。文献上的方法很多,目前各国药典较常用的有以下类型:(一)Lehmann氏类型;(二)Ewins氏类型;(三)Robertson氏类型;(四)Schulek及Villecz氏类型。这几类型中:(一)手续繁复且不能用于某些抗氧化力强之化合物;(二)(三)费时颇长,且操作中产生大量有害气体;(四)手续及时间虽较前三种简短,但操作稍有不慎,易得不一致结果。     

药品中砷盐限度测定的研究

本文对Gutzeit法测砷以及石灰法有机破坏的若干实验条件作了比较;并对中国药典新版拟收载需作砷检查的有机药品系统的逐个进行实验,分别选定其测砷时的处理方法。     

HG-AFS同时测定供水材料浸泡液中痕量砷和锑

供水材料浸泡液中砷、锑的测定,国家标准方法为采用比色法和石墨炉原子吸收法[1],两者都不能同时测定砷和锑。近年来,氢化物原子荧光法测定技术广泛应用于各个领域[2-5],本文用氢化物原子荧光法同时测定供水材料浸泡液     

锑剂和砷剂合并应用的毒性研究

酒石酸锑钾和葡萄糖酸锑钠均含有微量砷,各国对此二种锑剂中砷量限度的规定并不相同。本文对于微量砷影响锑剂毒性的问题,用小白鼠进行了比较系统的研究。结果表明当砷含量在200ppm以下时对二种锑剂的毒性无明显影响,仅当砷含量增至2000—20000ppm时二种锑剂的毒性始相应增加。同时按Loewe图解分析法用小白鼠分析酒石酸锑钾(PAT_sbⅢ)与三氧化二砷(AS^Ⅲ)和葡萄糖酸锑钠(SAG_sbv)与砷酸氢二钠(AS^v)合用时的毒性,证明PAT_sbⅢ与AS^Ⅲ间,SAG_sbv与AS^v 间的毒性均呈相加作用。     

微波消解-HG-AFS法测定不同产地中药材中砷和锑的含量

目的 建立微波消解-HG-AFS法同时测定中药材中砷和锑含量的方法.方法 采用微波消解的方法进行样品的前处理;用HG-AFS法同时测定中药材中砷和锑的含量.结果 砷、锑标准溶液进样量为0.8～10.0 ng,与峰面积呈良好线性关系,回归方程分别为Y=5.647X-0.957(r=0.999 8)和Y=310.851 X+13.256(r=0.999 8).样品中砷、锑平均回收率分别为97.20％和95.93％,RSD为1.56％、3.88％,样品中砷含量为0.002～4.849 mg/kg、锑含量为0.000 0～0.511 8 mg/kg.结论 本方法简便可行、分析速度快,适用于大批量快速测定中药材中的砷和锑.     

测定三碘(或四碘)甲状腺原氨酸钠中碘氨基酸杂质的反相高压液相层析法

美国药典规定用纸层析测定三碘甲腺氨酸钠(NaT_3)中二碘及四碘甲腺氨酸(T_2、T_3)杂质,但当杂质量很少时,该法不灵敏,不能准确测定;对四碘甲腺氨酸钠(MaT_4)尚无杂质检出方法。本文用反相高压液相层析法可在30分钟内准确、灵敏地测定标准品中小于75×10~(-12)克分子的杂质和分解产物。     

国内外药典右旋糖酐40原料药含氮量测定方法的比较

目的比较国内外药典中右旋糖酐40原料药含氮量测定的方法。方法分别采用《中国药典》(2010年版)、《美国药典》(USP-32)、《日本药局方》(JPⅩⅤ)、《英国药典》(BP 2010)和《欧洲药典》(EP 6.0)中右旋糖酐40原料药项下含氮物质的测定方法,对11批右旋糖酐40原料的含氮量进行分析。结果实验结果表明,《中国药典》所采用的纳氏比色法与国外药典所采用的的凯氏定氮法测定结果基本一致。结论纳氏比色法操作方法简单,作为限度检查时具有一定的实用价值;凯氏定氮法操作虽比较复杂,但定量测定结果更准确。     

氨磷汀HPLC测定方法的比较

比较了美国药典(USP 3 1)和中国部颁标准中氨磷汀的HPLC测定法.美国药典采用不同比例的乙腈-水(含全氟丁基磺酸或三氟乙酸)作为流动相,中国部颁标准则采用甲醇-3.5 mmol/L辛烷磺酸钠水溶液(磷酸调节pH 3.0)为流动相.两法均用外标法测定氨磷汀含量.测定有关物质时,美国药典用外标法测定硫醇含量,归一法测其它有关物质:中国部颁标准则用自身对照法测定有关物质含量.     

顶空进样气相色谱法测定中药酒剂中乙醇含量

中国药典(90版)规定乙醇量测定用气相色谱法.在测定中药酒剂的乙醇量时,发现有些中药酒剂所含中药成份多,浓度高.按药典法稀释后直接进样,样品中的固形物难以挥发,对色谱柱造成污染.本文采用顶     

锑的比色测定法 (一)用罗丹明-B试剂比色法的改进

在微量锑的定量法中,灵敏度高而反应专一的首推罗丹明-B 法。本反应首先由E.Eegriwe氏发现,用于锑化合物的定性试验,其后由 Fredrick,Webster 以及Fairhall 等人将它应用到定量方面;Maren 更把它引用到生物性检体内锑量的测定。虽然本反应发现和应用的历史已很久,而且在作为锑的定性试验时灵敏度很高,在操作技术上也毫无问题,但在用作微量锑的定量试验时,却存在着种种技术上的困难。按文献上现有的方法不能得到使人满意的结果。     

氢氧化钙法测定银杏叶片中的砷盐

目的建立测定银杏叶片中砷盐的方法。方法采用氢氧化钙法对样品中的有机物进行破坏,再用古蔡氏法测定砷盐含量。结果氢氧化钙法能够准确地测出银杏叶片中的砷盐。结论该方法准确,重现性好,空白试剂无干扰,可用于银杏叶片中砷盐的测定。     

有机砷药物的测定法

本文用三种药典法和两种改良法进行了有机砷化合物中砷含量的比较试验,证明所得结果是一致的,而以第四法为最简捷。此法系用硝酸硫酸进行有机破坏,加硫酸铵,在酸性液中以碘化钾处理,再用硫代硫酸钠溶液直接滴定。     

Arsenic-induced hepatic mitochondrial toxicity in rats and its amelioration by dietary phosphate

The present study was aimed to test the hypothesis that inorganic phosphate may reduce arsenic toxicity by decreasing its intestinal transference. Co-administration of inorganic phosphate (6.56 M) and arsenic (6.07 mM) in the intestinal loops of rats, in situ, caused significant reduction of arsenic transference. Short-term arsenic exposure (3mg/kg body weight/day for 30 days) caused liver damage evidenced by activities of liver enzymes and necroinflammatory changes. These effects of arsenic were coupled with enhanced mitochondrial swelling, inhibition of cytochrome c oxidase, Ca(2+)-ATPase, a decrease in mitochondrial calcium content, changes in indices of hepatic mitochondrial oxidative stress and iNOS expression. Arsenic also increased hepatic caspase 3 activity and DNA fragmentation. All these apoptosis-related molecular changes caused by arsenic could be alleviated by supplementation with inorganic phosphate, which likely suggests a protective role of phosphate against arsenic-induced hepatotoxic changes.     

Chelators as antidotes of metal toxicity: therapeutic and experimental aspects

The effects of chelating drugs used clinically as antidotes to metal toxicity are reviewed. Human exposure to a number of metals such as lead, cadmium, mercury, manganese, aluminum, iron, copper, thallium, arsenic, chromium, nickel and platinum may lead to toxic effects, which are different for each metal. Similarly the pharmacokinetic data, clinical use and adverse effects of most of the chelating drugs used in human metal poisoning are also different for each chelating drug. The chelating drugs with worldwide application are dimercaprol (BAL), succimer (meso-DMSA), unithiol (DMPS), D-penicillamine (DPA), N-acetyl-D-penicillamine (NAPA), calcium disodium ethylenediaminetetraacetate (CaNa(2)EDTA), calcium trisodium or zinc trisodium diethylenetriaminepentaacetate (CaNa(3)DTPA, ZnNa(3)DTPA), deferoxamine (DFO), deferiprone (L1), triethylenetetraamine (trientine), N-acetylcysteine (NAC), and Prussian blue (PB). Several new synthetic homologues and experimental chelating agents have been designed and tested in vivo for their metal binding effects. These include three groups of synthetic chelators, namely the polyaminopolycarboxylic acids (EDTA and DTPA), the derivatives of BAL (DMPS, DMSA and mono- and dialkylesters of DMSA) and the carbodithioates. Many factors have been shown to affect the efficacy of the chelation treatment in metal poisoning. Within this context it has been shown in experiments using young and adult animals that metal toxicity and chelation effects could be influenced by age. These findings may have a bearing in the design of new therapeutic chelation protocols for metal toxicity.     

快速湿氧化法的研究 Ⅲ.有机砷药物中砷的含量测定

用快速湿氧化法破坏半微量的样品后,可用碘量法定量地回收五价砷。六种有机砷药物的定量結果与标准方法一致。抗氧化力較强的苯胂酸也能順利地破坏,得到一致的結果,伹不能破坏二甲胂酸.对氧化剂（高錳酸鉀-浓硫酸溶液)破坏有机貭的特性进行了試驗,結果訊为爆鳴系由高錳酸酐(Mn₂O₇)在液面处剧烈分解所致。建議使用浓度为7%以下的氧化剂。先将适量的高錳酸鉀粉末加进样品溶液,再以适量氧化剂溶液处理,可破坏大量有机貭而不引入过多的硫酸。     

肾骨颗粒中几种成分的含量测定

目的测定肾骨颗粒中多种成分的含量,为其质量评价提供理论依据。方法分别采用滴定法、苯酚硫酸法、氨基酸自动分析法、比色法、古蔡法、原子吸收分光光度法、钼蓝分光光度法对肾骨颗粒中的醋酸钙、多糖、氨基酸、重金属、砷、铅、磷进行含量测定。结果肾骨颗粒中醋酸钙的含量为48.17%,多糖含量为2.14%, 氨基酸含量为3.32%,磷含量为2.4×10－6,重金属总量≤1.0×10－6,砷含量≤2.0×10－6,铅含量≤0.5×10－6。 结论肾骨颗粒营养成分含量高,有害成分含量很低,质量良好。     

Arsenic trioxide in environmentally and clinically relevant concentrations interacts with calcium homeostasis and induces cell type specific cell death in tumor and non-tumor cells

While arsenic compounds are known as environmental toxicants (especially in drinking water) and as carcinogens, some arsenic compounds, like arsenic trioxide (As2O3), are clinically used in humans to treat some forms of cancer (e.g. leukemia). Although arsenic compounds have been studied intensively, their interactions with living cells are still not fully elucidated. We have previously proposed that modulation of intracellular calcium ([Ca2+]i) homeostasis induced by As2O3 could be an important mechanism to induce cytotoxicity. Here we demonstrate, using human cell models (neuroblastoma (SY-5Y) or embryonic kidney cells (HEK)) and confocal microscopy in combination with the calcium sensitive dye fluo 4-AM, that As2O3 interferes with calcium signaling at low (environmentally and clinically relevant concentrations of 100 pM to 1 microM). Within this concentration range, As2O3 had cell type specific cytotoxic effects, with neuroblastoma cells being more sensitive to As2O3 than HEK 293. In addition, by staining with Hoechst 33347 and counting micronucleated cells as well as apoptotic nuclei, As2O3 was found to increase the rate of apoptosis and DNA damage, which was also cell type specific. These results indicate that the As2O3-induced cell death could be triggered or mediated by [Ca2+]i signals and suggest that low concentrations of As2O3 are able to interfere with specific physiological processes in diverse cell models.     

Arsenic-induced oxidative stress and its reversibility following combined administration of N-acetylcysteine and meso 2,3-dimercaptosuccinic acid in rats

1. The present study examined whether arsenic induces oxidative stress in liver, brain and erythrocytes (RBC) based on the investigation of certain selected parameters. It also explored the possibility that combined administration of N-acetylcysteine (NAC) and meso 2,3-dimercaptosuccinic acid (DMSA) was capable of achieving better reversibility in the parameters indicative of arsenic-induced oxidative stress than individual treatment with either of these drugs. 2. Male rats were exposed to 100 p.p.m. sodium arsenite in their drinking water for 12 weeks (equivalent to 12 mg/kg As). The arsenic was then removed and rats were given NAC (1 mmol/kg per day), DMSA (1 mmol/kg per day) or a combination of the two, orally, once daily for 5 days. Animals not given arsenic and those given arsenic but not NAC or DMSA served as negative and positive controls, respectively. 3. Twelve weeks of arsenic exposure was found to deplete glutathione (GSH) levels, increase oxidized glutathione (GSSG) and promote malondialdehyde (MDA) production in both liver and brain samples. In addition to a significant reduction in RBC delta-aminolevulinic acid dehydratase (ALAD) activity and GSH levels, a marked elevation in MDA production may also contribute to arsenic-induced oxidative stress. 4. Treatment with either NAC or DMSA alone partially reversed arsenic-induced alterations in hepatic GSH and MDA, while only brain MDA levels responded favourably to these drugs. Only DMSA appeared to restore blood ALAD, while RBC MDA levels responded favourably to both drugs. Treatment with DMSA also produced an effective depletion of blood and hepatic arsenic concentrations. In the liver, most of these parameters were more effectively reversed by combined treatment with NAC and DMSA compared with the effects of either drug alone. 5. These results provide in vivo evidence of arsenic-induced oxidative stress in liver, brain and RBC and indicate that these effects can be mitigated by pharmacological intervention that encompasses combined treatment with NAC and DMSA.