慢性砷暴露对人皮肤角质形成细胞药物转运相关蛋白mRNA表达和砷代谢的影响

目的探讨慢性砷暴露对人皮肤角质形成细胞(human keratinocytes,HaCaT)药物转运蛋白mRNA表达和砷代谢的影响。方法将HaCaT细胞随机分为慢性对照(不予以砷处理)组和慢性砷暴露(100 nmol/L亚砷酸钠染毒28周)组,培养于含10%胎牛血清和1%双抗的培养基中,收集处于对数生长期的细胞,采用实时荧光定量(real-time quantitative PCR)法检测细胞多药耐药相关蛋白mRNA的表达水平。将处于对数生长期的HaCaT对照细胞和慢性砷暴露细胞分别暴露于含终浓度为0(对照)、2.5、5、10、20、30、40、50、60、80、100、150μmol/L亚砷酸钠的培养基中孵育24 h,采用MTS法检测细胞活性。将慢性砷暴露组细胞和对照细胞予以10μmol/L亚砷酸钠处理24 h,采用氢化物发生-原子吸收分光光度法检测细胞砷蓄积和砷排放量。结果与对照细胞相比,慢性砷暴露HaCaT细胞多药耐药相关蛋白ABCC2和ABCC4 mRNA表达水平均升高,差异有统计学意义(P0.05);而ABCC1、ABCC3、ABCC5、ABCG1、ABCG2 mRNA的表达水平均无显著变化。与对照细胞相比,慢性砷暴露HaCaT经各浓度急性砷处理后细胞存活率均升高,差异有统计学意义(P0.05)。与对照细胞相比,10μmol/L亚砷酸钠染毒24 h后,慢性砷暴露细胞内的砷蓄积量降低,而砷排放量升高,差异均有统计学意义(P0.05)。结论慢性砷暴露的HaCaT细胞药物转运蛋白mRNA的表达升高,砷排出能力增强,对砷毒性产生耐受性。     

砷及其代谢产物对P21基因表达的影响

目的探讨砷及砷化物对人肺腺癌细胞系A549细胞、云南宣威肺腺癌细胞XWLC-05细胞、人乳腺癌细胞MDAMB-231细胞中的P21基因表达的影响。方法以亚砷酸钠、一甲基砷酸(MMA)、二甲基砷酸(DMA)处理A549细胞、XWLC-05细胞、MDA-MB-231细胞并以荧光定量聚合酶链式反应(q RT PCR)法检测P21mRNA的表达;以不同浓度的亚砷酸钠处理A549细胞、XWLC-05细胞、MDA-MB-231细胞并以q RT PCR法检测P21基因mRNA的表达。结果亚砷酸钠可诱导P21基因mRNA的表达,MMA、DMA不能诱导细胞中P21基因m RNA的表达;不同的亚砷酸浓度处理的细胞,可影响细胞中P21基因mRNA的表达。结论砷可影响细胞中P21基因的表达,并且与剂量存在一定的关系。     

硫酸镍与亚砷酸钠联合致叙利亚地鼠胚胎细胞转化作用的实验研究

目的　探讨砷在镍冶炼工肺癌病因中的作用。方法　采用细胞灶法观察硫酸镍与亚砷酸钠联合致叙利亚地鼠胚胎 (SHE)细胞的形态学转化作用。结果　硫酸镍、亚砷酸钠及硫酸镍与亚砷酸钠联合染毒三个组均有细胞转化灶形成 ,其形成率均呈现剂量依赖关系。刀豆球蛋白A凝集试验进一步验证了细胞转化结果。联合作用分析显示 ,硫酸镍为 2 .5 μg/ml,亚砷酸钠分别为 0 .12 5、0 .2 5 0、0 .5 0 0和 1.0 0 0 μg/ml,两化合物联合作用转化率实测值分别为 1.44 %、2 .34 %、3.30 %和3.94% ,而预期转化率分别为 1.78%、2 .2 2 %、3.38%和 3.37%。说明在等剂量原则下 ,硫酸镍、亚砷酸钠单独染毒的转化细胞灶形成率之和与两化合物同时染毒的转化细胞灶形成率非常接近 ;析因分析未见两者间有交互作用 (P =0 .6 16 )。结论　Ni2 、As3 具有细胞转化活性 ,二者联合呈相加作用。     

^60Coγ射线诱发的V79细胞HPRT位点突变频率

用中国仓鼠Ｖ７９细胞次黄嘌呤－鸟嘌呤磷酸核糖基转移酶（ＨＰＲＧ）位点正向突变试验方法（Ｖ７９／ＨＰＲＴ ＳＹＳＴＥＭ）检测了不同剂量的＾６Ｃｏ－ｙ射线诱发的Ｖ７９细胞ＨＰＲＴ位点的突变频率。     

亚砷酸钠对雄性小鼠的生殖毒性作用

目的 探讨亚砷酸钠对雄性生殖细胞生殖毒性的影响.方法 选用雄性小鼠染砷,分批与正常雌性小鼠交配,观察雄性小鼠生精细胞发育不同阶段砷毒对受孕率、胚胎死亡率及体细胞嗜多染红细胞致突性的影响效应.结果 染砷后第2、4周30 mg/kg剂量组受孕率低于70%;染砷后第6周10、15、30 mg/kg组胚胎死亡率分别为30.0%、38.9%、40.0%,仍明显高于阴性对照组16.7%;染砷剂量>10 mg/kg时,周围血体细胞嗜多染红细胞致突性损伤恢复时间早于生殖细胞致突性损伤恢复时间.结论 亚砷酸钠可作用于观察期内生精细胞发育的各个环节,以对精细胞发育作用最为明显,主要表现为受孕率随染毒剂量增加而降低,胚胎死亡率随剂量的增加而升高.     

砷对人正常膀胱上皮细胞信号传导与转录激活因子3mRNA表达的影响

目的研究亚砷酸钠对人正常膀胱上皮(SV-HUC-1)细胞中信号传导与转录激活因子3(STAT3)m RNA表达的影响。方法将处于对数生长期的SV-HUC-1细胞分别进行急性染毒[暴露于含终浓度为0(对照)、1、2、4、8、10μmol/L亚砷酸钠的培养基染毒24 h]和慢性染毒[以含终浓度为0(对照)、0.5μmol/L亚砷酸钠的培养基染毒40代]。采用逆转录PCR(RT-PCR)方法检测细胞STAT3 m RNA表达情况。结果与对照组比较,4、8、10μmol/L亚砷酸钠暴露组SV-HUC-1细胞内STAT3 m RNA的表达水平均升高,差异均有统计学意义(P0.05);且随着亚砷酸钠染毒剂量的升高,SV-HUC-1细胞内STAT3 m RNA的表达水平呈先升高后下降的趋势。0.5μmol/L亚砷酸钠慢性暴露组SV-HUC-1细胞内STAT3m RNA的表达水平高于对照组,差异有统计学意义(P0.05)。结论砷可能通过调控STAT3的表达而在砷诱导的SVHUC-1细胞恶性转化中发挥一定作用。     

硫酸镍与亚砷酸钠联合致叙利亚地鼠胚胎细胞转化作 …

目的 探讨砷在镍治炼工肺癌病因中的作用。方法 采用细胞灶法观察硫酸镍与亚砷酸联 合致叙利亚地鼠胚胎（ＳＨＥ）细胞的形态学转化作用。结果 硫酸镍、亚砷酸钠及硫酸镍与亚砷酸钠联合染毒三个组均有细胞转化灶形成,其形成率均呈现剂量依赖关系。刀豆球蛋白Ａ凝集试验进一步验证了细胞转化结果。联合作用分析显示,硫酸镍为２．５ug/ml,亚 砷酸钠分别为０．１２５、０．２５０、０．５００和１．０００ug/ml,两化合物联合作     

不同价态无机砷染毒大鼠肝脏砷形态分析

目的通过观察不同价态无机砷染毒大鼠肝脏砷形态代谢产物分布,初步探讨不同价态无机砷体内代谢和毒性机制。方法 W istar大鼠42只,随机分成7组,于染砷3个月后,处死动物,迅速摘取肝脏,于-80℃冷藏;采用高效液相色谱-氢化物发生原子荧光光谱法(HPLC-HGAFS)测定并比较各组染砷大鼠肝脏中砷形态代谢产物的水平和分布,计算一甲砷酸(MMA)加标回收率评价结果准确度;通过肝脏中总砷含量评价砷蓄积能力;分析肝脏中甲基化代谢指标一甲基化率(PM I)和二甲基化率(SM I)水平,评价各组间甲基化代谢能力或途径差异。结果亚砷酸钠与砷酸钠高、中、低剂量组总砷水平分别为(1 142.9±50.4)、(484.6±37.4)、(323.3±20.2)和(3 695.2±345.9)、(1833.8±229.6)、(1 170.5±77.4)ng/g,砷酸钠各剂量组总砷水平明显高于亚砷酸钠组(P<0.05);亚砷酸钠中、低剂量组iAs3+[(118.4±23.9)、(252.3±14.3)]ng/g和二甲砷酸(DMA)[(353.2±45.6)、(55.2±10.6)]ng/g含量均低于砷酸钠组(P<0.05);亚砷酸钠...     

无机砷对人皮肤成纤维细胞增殖毒性的实验观察

目的观察亚砷酸钠诱导体外培养的人皮肤成纤维细胞的作用，探讨砷性皮肤损伤的分子机制。方法通过直接细胞计数法和噻唑蓝（MTT）还原法检测亚砷酸钠对皮肤成纤维细胞生长的影响。结果与对照组比较，皮肤成纤维细胞经不同剂量的亚砷酸钠诱导后，吸光度值均有改变，存在剂量效应关系（P〈0.01）。0．5～5．0μmol／L浓度的亚砷酸钠对皮肤成纤维细胞有明显的增殖作用，而10μmol／L浓度的亚砷酸钠产生明显的毒性作用。结论低浓度NaAsO2、NaAsO2刺激人皮肤成纤维细胞增殖，高浓度具有细胞毒性。     

亚慢性饮水砷暴露小鼠组织形态砷的蓄积与分布

目的探讨亚慢性饮水砷暴露小鼠各组织中无机砷及其代谢产物的蓄积与分布规律。方法将40只健康8周龄清洁级昆明雌性小鼠按体重随机分为对照(生理盐水)组和50、100、200 mg/L亚砷酸钠染毒组,每组10只。采用亚砷酸钠自由饮水方式染毒,连续染毒3个月。检测小鼠肝脏、肾脏、脾脏、肺脏、膀胱、大脑皮层、小脑和海马组织中五价无机砷(pentavalent inorganic arsenic,iAs~(5+))、三价无机砷(trivalent inorganic arsenic,iAs~(3+))、单甲基胂酸(monomethylated arsenic,MMA)和二甲基胂酸(dimethylated arsenic,DMA)的含量,并计算总砷(total arsenic,TAs)含量。结果各浓度亚砷酸钠暴露组小鼠肝脏中TAs、iAs~(3+)和DMA的含量与对照组比较,差异均无统计学意义(P0.05)。与50 mg/L亚砷酸钠暴露组比较,100、200 mg/L亚砷酸钠暴露小鼠肾脏、肺脏和膀胱中TAs和DMA含量均升高,差异有统计学意义(P0.05);与100 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露小鼠肾脏TAs和DMA含量均升高,差异有统计学意义(P0.05)。与50 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露小鼠脾脏TAs和DMA含量以及膀胱iAs~(3+)含量均升高,差异有统计学意义(P0.05)。与100 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露小鼠膀胱TAs、iAs~(3+)和DMA含量均升高,差异有统计学意义(P0.05)。与50 mg/L亚砷酸钠暴露组比较,100 mg/L亚砷酸钠暴露小鼠大脑皮层和小脑中TAs含量及200 mg/L亚砷酸钠暴露小鼠大脑皮层和小脑中TAs和DMA的含量均升高,差异有统计学意义(P0.05);与100 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露小鼠小脑TAs和DMA含量均升高,差异有统计学意义(P0.05)。与50 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露小鼠海马TAs、MMA和DMA含量均升高,差异有统计学意义(P0.05);与100 mg/L亚砷酸钠暴露组比较,200 mg/L亚砷酸钠暴露小鼠海马MMA含量升高,差异有统计学意义(P0.05)。各浓度亚砷酸钠暴露组小鼠组织中iAs~(3+)以及肺脏和膀胱中MMA的含量间比较,差异均无统计学意义(P0.05)。随着亚砷酸钠暴露浓度的升高,小鼠各组织中TAs和DMA含量均呈上升趋势,膀胱和海马中MMA亦呈上升趋势。100、200 mg/L亚砷酸钠暴露组小鼠各组织中TAs和DMA的含量由高到低依次为膀胱肝脏肺脏肾脏脾脏;部分脑区组织中TAs和DMA的含量由高到低依次为大脑皮层海马小脑。200 mg/L亚砷酸钠暴露组小鼠肺脏、100和200 mg/L亚砷酸钠暴露组小鼠膀胱以及50、100和200 mg/L亚砷酸钠暴露组小鼠海马中可检测出MMA,其它各浓度亚砷酸钠暴露组小鼠组织中MMA均未检出所有亚砷酸钠暴露组小鼠组织中均未检出iAs~(5+)。结论亚慢性饮水砷暴露小鼠组织中形态砷的蓄积与分布具有明显的组织特异性,并且无机砷及其代谢产物能够穿越血脑屏障,区域特异性地蓄积在大脑皮层、小脑和海马组织。     

无机砷对人皮肤成纤维细胞缝隙连接通讯的影响

目的 探讨无机砷对人皮肤成纤维细胞缝隙连接通讯的影响。方法 采用细胞划痕染料标记示踪技术,以荧光染料在细胞间的扩散作为评价缝隙连接通讯的指标,观察亚砷酸和砷酸对原代培养的人皮肤成纤维细胞缝隙连接通讯的影响。结果 亚砷酸可显抑制人皮肤成纤维细胞间荧光黄染料的扩散,在0．005-5．0μmol／L浓度范围内有明显的剂量依赖关系。砷酸也可明显抑制荧光黄染料在人皮肤成纤维细胞间的扩散,但剂量依赖关系不明显。进一步的研究发现,亚砷酸可显增高人皮肤成纤维细胞胞膜和胞浆蛋白激酶C的活性,其中对胞膜蛋白激酶C活性的作用更为明显。结论 无机砷可显抑制人皮肤成纤维细胞缝隙连接通讯,提示它们在癌症发生的促长阶段扮演重要角色。无机砷对细胞缝隙连接通讯的抑制可能与其引起细胞内蛋白激酶C的异常活化有关。     

Metabolites of Arsenic Induced Tetraploids and Mitotic Arrest in Cultured Cells

The toxic effects of arsenic compounds on cell division were studied, using Chinese hamster V79 cells. Seven arsenic compounds were tested. Inorganic arsenic compounds (arsenite and arsenate), which have been found in drinking water, inhibited cell growth at very low concentrations. Monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), and trimethylarsine oxide (TMAO), which are methylated metabolites of inorganic arsenics, were less cytotoxic than the inorganic arsenics themselves. The cytotoxicity of the three methylated metabolites decreased as the number of methyl groups increased. Arsenobetaine (AsBe) and arsenocholine (AsC), which have been found in some marine products, did not show any cytotoxicity. Three methylated metabolites; MMA, DMA and TMAO induced mitotic arrest. Tetraploidy production was observed in cells exposed to DMA or TMAO. Arsenite, arsenate, AsBe and AsC did not induce mitotic arrest or tetraploids. These results suggest that MMA, DMA and TMAO exert some effect on cell division in metaphase and may thereby give some clue as to the carcinogenic mechanism of arsenic. Received: 9 April 1996/Revised: 15 June 1996     

Quantitative Study of As (V) and As (III) Interaction with Mangrove DNA by Molecular Fluorescence Spectroscopy

This study describes the in vitro study of (1:1) one step nucleophilic displacement ( \({\text{S}}_{\text{N}}^{1}\) ) of phosphate by heavier anion arsenate and arsenite in the DNA of arsenic ridden Sundarban mangroves. Mangrove DNA was found to give rise to a broad fluorescence and its integrated fluorescence intensity was enhanced on addition of As (V) and As (III), respectively. Analyses of the fluorescence parameter showed adequacy of 1:1 model to describe substitution of phosphate of mangrove DNA chain exiplex by arsenate and arsenite with equilibrium constant (log K_c) ranging between 4.19 and 4.32 for As (V), and between 3.77 and 3.89 for As (III) at pH 7 and 25°C. In the cases, the melting temperature (T_m) and reassociation rate constant of mangrove DNA was increased on treatment with As (V) and As (III). It is suggested that heavier ion arsenate and arsenite may substitute phosphate in natural DNA.     

Concentration and chemical status of arsenic in the blood of pregnant hamsters during critical embryogenesis. 2. Acute exposure

We have determined the concentration and chemical composition of arsenic in the blood of pregnant hamsters between 0.2 and 6 hr after an intraperitoneal injection of a teratogenic dose of radiolabeled sodium arsenate on the morning of the eighth day of gestation. Arsenic was present in plasma and red cells 0.20 hr postinjection. The plasma arsenic concentration reached a maximum of 220 mumole/kg blood near 0.5 hr postinjection. Plasma arsenic existed entirely as low-molecular-weight species. Both arsenite and dimethylarsinate (DMA) were present in plasma 0.20 hr postinjection, indicating that arsenate reduction and methylation of arsenic are rapidly initiated. However, the arsenite contribution remained small while the DMA contribution increased with time. Red cell arsenic included macromolecular arsenic (AsP) as well as three low-molecular-weight forms. The contribution of DMA remained small, but arsenite and AsP contributions increased with time. These findings identify the maternal blood concentration and chemical status of arsenic following the administration of a teratogenic dose of arsenate during the period of organogenesis. They could prove useful for predicting the likelihood of a teratogenic outcome in other mammalian species.     

Removal and transport mechanisms of arsenics in UF and NF membrane processes

In this study, the removal and transport mechanisms of ionized and non-ionized arsenics through NF and UF membranes were systemically investigated. The charge repulsion between the membrane surface and arsenic ions was an important mechanism for the rejection of ions by a charged membrane. In addition, the effect of J0/k ratio was dependent on the membrane and ion charge, but the cross-flow velocity was not significantly affected. Both diffusion and convection are proved to affect the transport of arsenic ions. The reflection coefficients (sigma) of both UF and NF membranes increased with increasing pH; the reflection coefficients of arsenate were higher than those of arsenite under the same operating conditions. The spiral-wound module exhibited slightly higher arsenate removal than the flat-sheet module under the same operating conditions.     

Acute toxicity of thioarsenates to Vibrio fischeri

Thioarsenic species often are the predominant arsenic species in sulfidic environments, yet little is known about their toxicity. We report to our knowledge the first determination of acute toxicity of mono-, di-, and trithioarsenate to the bioluminescent bacterium Vibrio fischeri, which increases with an increasing number of thio(SH)-groups. Whereas mono- and dithioarsenate are much less toxic (effective analyte concentration causing a 50% decrease in luminescence [EC50], 676 and 158 mg/L, respectively), the toxicity of trithioarsenate (EC50, 14.4 mg/L) is comparable to the toxicities of arsenate and arsenite (EC50, 9.1 and 26.1 mg/L, respectively). The low toxicity of monothioarsenate is remarkable, because it has chemical properties very similar to those of arsenate. In contrast to the toxicities of arsenite and arsenate, the toxicity of thioarsenates increases with exposure time, suggesting a lack of detoxification mechanisms or a conversion of thioarsenic species into arsenic oxyanions after uptake. We determined the acute toxicity of synthetic arsenite solutions with varying sulfide concentration to V. fischeri. Arsenic speciation in these solutions was measured by ion chromatography-inductively coupled plasma-mass spectrometry, and the observed toxicity was related to the different arsenic species present. High inhibition of luminescence was observed at low and high ratios of sulfur to arsenic, in which arsenite or a mixture of di-, tri-, and tetrathioarsenate dominated arsenic speciation. Acute toxicity decreased at sulfur to arsenic ratios of from 1 to 10, with a minimum luminescence inhibition of 30% at a ratio of 3.5, at which concentrations of 55 mg/L of arsenite and 30 mg/L of trithioarsenate were determined. The toxicity observed under these conditions is much lower than that anticipated from the individual dose-response curves that predict each species alone already should cause 70 to 80% inhibition. The low toxicity suggests an antagonistic toxicological interaction between arsenite and trithioarsenate.     

Arsenic biotransformation by the brown macroalga, Fucus serratus

The brown alga Fucus serratus was maintained in aquaria with added arsenate (0, 20, 50, and 100 microg As/L, four individuals per treatment) for up to 19 weeks. Biotransformation of arsenic by Fucus was monitored by high-performance liquid chromatography/inductively coupled plasma mass spectrometry and liquid chromatography/electrospray mass spectrometry analysis of aqueous extracts of algal frond tips removed periodically throughout the experiment. Major arsenic species monitored were arsenate, arsenite, methylarsonate, dimethylarsinate, and the four arsenosugars 1 to 4 found naturally in Fucus. Algae accumulated arsenate readily and transformed it into several arsenic compounds depending on the exposure concentration. At 100 microg As/L, the major metabolite was arsenite with smaller quantities of methylarsonate and dimethylarsinate, but only traces of arsenosugars were formed. In contrast, the 20-microg-As/L group accumulated only small quantities of arsenite and methylarsonate, while dimethylarsinate and arsenosugars were major arsenic metabolites. At 50 microg As/L exposure, algae had significant quantities of all arsenic metabolites monitored. Arsenate was toxic to the algae at 100 microg As/L but had no obvious detrimental effect at 20 microg As/L. The data are consistent with a process of arsenate detoxification by reduction and alkylation; at higher exposures, however, the alkylation processes become saturated, leading to an accumulation of arsenite and subsequent toxicity.     

Response of Pepper Plants (<Emphasis Type="Italic">Capsicum annum</Emphasis> L.) on Soil Amendment by Inorganic and Organic Compounds of Arsenic

The influence of soil contamination by inorganic and organic arsenic compounds on uptake, accumulation, and transformation of arsenic in pepper (Capsicum annum L.) was investigated in greenhouse pot experiments under controlled conditions. Pepper plants were cultivated in substrate amended by aqueous solutions of arsenite, arsenate, methylarsonic acid (MA), and dimethylarsinic acid (DMA) applied individually into cultivation substrate at concentrations of 15 mg As per kg of substrate. The plant availability of the arsenicals increased in the order arsenite = arsenate < MA < DMA. The highest arsenic concentrations were found in roots followed by stems, leaves, and fruits regardless of arsenic compound applied. In the control samples of pepper fruits, As(III), As(V), and DMA were present (25%, 37%, and 39% of the water-extractable arsenic). In control stems + leaves and roots, As(V) was the major compound (63% and 53% in a phosphate buffer extract) followed by As(III) representing 33% and 42%. Additionally, low concentrations (not exceeding 5%) of DMA and MA were detected as well. In all the soils analyzed after the first harvest of pepper fruits, arsenate was the dominating compound followed by arsenite. Methylarsonic acid, methylarsonous acid, and DMA were present at varying concentrations depending on the individual soil treatments. In the treated plants, the arsenic compounds in plant tissues reflected predominantly the extractable portions of arsenic compounds present in soil after amendment, and this pattern was more significant in the first part of vegetation period. The results confirmed the ability of generative parts of plants to accumulate preferably organic arsenic compounds, whereas in the roots and aboveground biomass, mainly inorganic arsenic species are present. Evidently, the source of soil arsenic contamination affects significantly the extractable portions of arsenic compounds in soil and subsequently the distribution of arsenic compounds within the plants.     

Determination of monomethylarsonous acid, a key arsenic methylation intermediate, in human urine

In this study we report on the finding of monomethylarsonous acid [MMA(III)] in human urine. This newly identified arsenic species is a key intermediate in the metabolic pathway of arsenic biomethylation, which involves stepwise reduction of pentavalent to trivalent arsenic species followed by oxidative addition of a methyl group. Arsenic speciation was carried out using ion-pair chromatographic separation of arsenic compounds with hydride generation atomic fluorescence spectrometry detection. Speciation of the inorganic arsenite [As(III)], inorganic arsenate [As(V)], monomethylarsonic acid [MMA(V)], dimethylarsinic acid [DMA(V)], and MMA(III) in a urine sample was complete in 5 min. Urine samples collected from humans before and after a single oral administration of 300 mg sodium 2,3-dimercapto-1-propane sulfonate (DMPS) were analyzed for arsenic species. MMA(III) was found in 51 out of 123 urine samples collected from 41 people in inner Mongolia 0-6 hr after the administration of DMPS. MMA(III )in urine samples did not arise from the reduction of MMA(V) by DMPS. DMPS probably assisted the release of MMA(III) that was formed in the body. Along with the presence of MMA(III), there was an increase in the relative concentration of MMA(V) and a decrease in DMA(V) in the urine samples collected after the DMPS ingestion.     

Isolation of Arsenite-Oxidizing Bacteria from Arsenic-Enriched Sediments from Camarones River,Northern Chile

In Northern Chile, high arsenic concentrations are found in natural water, both natural and anthropogenic sources, a significant health risk. Nine bacterial strains were isolated from Camarones river sediments, located in Northern Chile, a river showing arsenic concentrations up to 1,100 μg/L. These strains were identified as Pseudomonas and they can oxidize arsenite (As(III)) to the less mobile arsenate (As(V)). The arsenite oxidase genes were identified in eight out of nine isolates. The arsenite oxidizing ability shown by the nine strains isolated from arsenic enriched sediments open the way to their potential application in biological treatment of effluents contaminated with arsenic.