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二甲基砷暴露大鼠尿中多形态砷检测分析

Determination and evaluation of arsenic speciation in urine of rat exposed to dimethyl arsenic
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摘要 目的观察饮用含不同浓度二甲基砷(DMA)水大鼠尿中砷化物的代谢情况。方法初断乳健康Wistar大鼠36只,雌鼠体质量(60±5)g,雄鼠体质量(50±5)g,按体质量将大鼠随机分为对照组、低剂量组、高剂量组,每组12只大鼠(雌雄各半)。低剂量组和高剂量组大鼠分别饮用含100、200mg/LDMA的水,对照组大鼠饮用蒸馏水。染毒10周后,采用氢化物发生原子吸收分光光度法测定大鼠尿中无机砷(iAs)、一甲基砷(MMA)、二甲基砷(DMA)和三甲基砷(TMA)。结果染毒10周后,对照组,低剂量组,高剂量组大鼠尿中iAs、MMA、DMA、TMA含量中位数比较差异有统计学意义(X。值分别为25.441、25.942、25.751、17.767,P均〈0.01)。其中低剂量组大鼠尿中iAs、MMA、DMA含量中位数(2.541、4.383、24.447mg/L)均高于对照组(0.784、0.000、0.743mg/L,P均〈0.05],高剂量组大鼠尿中iAs、MMA、DMA、TMA含量中位数(3.978、7.186、35.112、4.518mg/L)均高于对照组(0.784、0.000、0.743、0.000mg/L,P均〈0.05),且随染毒剂量的增加而升高(P〈0.05)。结论大鼠暴露DMA,大部分以原型从尿中排出,小部分可代谢转化为TMA。 Objective To observe the distribution and metabolism of arsenic speciation in urine of rats exposed to different concentrations of dimethylaraenic acid (DMA) through drinking water. Methods Thrity six weaning Wistar rats were randomly divided into normal control, low-dose group and high-dose group, 12 rats in each group(6 female and 6 male); average body weight of female rats was (60 ± 5)g, and male rats was (50 + 5)g. All rats of the 3 groups were given DMA at concentrations of 0, 100, 200 mg/L, respectively, corresponding to their specific groups through drinking water for 10 weeks. Inorganic arsenic (iAs), monomethylarsenic acid (MMA), DMA and trimethylarsenic compound(TMA) in urine were measured by hydride generation trapping and ultra- hypothermia coupled with atomic absorption spectrometry. Results After feeding for 10 weeks, the differences of rat urinary concentrations of iAs, MMA, DMA and TMA between normal control, low-dose group and high-dose group were statistically significant(x^2 = 25.441, 25.942, 25.751, 17.767, all P〈 0.01). Urinary concentrations of iAs, MMA and DMA(2.541, 4.383, 24.447 mg/L) of low-dose group were significant higher than those of normal control (0.784, 0.000, 0.743 mg/L, all P 〈 0.05) ; iAs, MMA, DMA and TMA(3.978, 7.186, 35.112, 4.518 mg/L) of high-dose group were significantly higher than those of normal control (0.784, 0.000, 0.743, 0.000 mg/L, all P 〈 0.05). The concentrations increased along with increasing doses of DMA concentrations in drinking water(all P 〈 0.05). Conclusions After rats are exposed to DMA, most of the DMA are excreted in unchanged form in urine and a small portion of DMA is metabolized into TMA.
出处 《中华地方病学杂志》 CAS CSCD 北大核心 2013年第6期629-631,共3页 Chinese Journal of Endemiology
基金 国家自然科学基金
关键词 二甲基砷酸 甲基化 大鼠 尿 Dimethylaraenic acid Methylation Rats Urine
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参考文献13

  • 1李昕,孙贵范.慢性饮水型砷中毒人群发、尿、血砷含量及皮肤色素细胞改变特点[J].中国地方病防治,2007,22(6):403-406. 被引量:11
  • 2Hughes MF,Beck BD,Chen Y. Arsenic exposure and toxicology:a historical perspective[J].Toxicological Sciences,2011,(02):305-332.
  • 3Jomova K,Jenisova Z,Feszterova M. Arsenic:toxicity,oxidative stress and human disease[J].Journal of Applied Toxicology,2011,(02):95-107.
  • 4Naujokas MF,Anderson B,Ahsan H. The broad scope of health effects from chronic arsenic exposure:update on a worldwide public health problem[J].Environmental Health Perspectives,2013,(03):295-302.
  • 5Sun G. Arsenic contamination and arsenicosis in China[J].Toxicology and Applied Pharmacology,2004,(03):268-271.
  • 6Hayakawa T,Kobayashi Y,Cui X. A new metabolic pathway of arsenite arsenic-ghtathione complexes are substrates for human arsenic methyltransferase Cyt 19[J].Archives of Toxicology,2005,(04):183-191.
  • 7Aposhian HV,Zakharyan RA,Avram MD. A review of the enzymology of arsenic metabolism and a new potential role of hydrogen peroxide in the detoxication of the trivalent arsenic species[J].Toxicology and Appiled Pharmacology,2004,(03):327-335.
  • 8Yamamoto S,Konishi Y,Matsuda T. Cancer induction by an organic arsenic compound,dimethylarsinic acid(cacodylic acid),in F344/DuCrj rats after pretreatment with five arcinogens[J].Cancer Research,1995,(06):1271-1276.
  • 9Wei M,Wanibuchi H,Yamamoto S. Urinary bladder carcinogenicity of dimethylarsinic acid in male F344 rats[J].Carcinogenesis,1999,(09):1873-1876.
  • 10Yamauchi H,Yamamura Y. Metabolismand excretion of orally administered dimethylarsinic acid in the hamster[J].Toxicology and Applied Pharmacology,1984,(01):134-140.

二级参考文献9

  • 1Yoshida T, Yamauchi H, Sun GF. Chronic health effects in people exposed to arsenic via the drinking water: dose - response relationships in review[ J]. Toxicol Appl Pharmacol, 2004,198 ( 3 ) :243 - 252.
  • 2Sun G, Li X, Pi J, et al. Current research problems of chronic arsenicosis in China[ J]. J Health Popul Nutr, 2006,24 (2) :176 - 181.
  • 3Walvekar PR, Kane SV, Nadkami MS, et al. Chronic arssenic poisoning: a gloval health issue - a report of multiple primary cancers [ J ]. J Cutan Pathol, 2007,34 ( 2 ) :203-206.
  • 4Yamauchi H, Yamamura Y. Metabolism and excretion of orally administered dimethylarsinic acid in the hamster [ J ]. Toxicol Appl Pharmacol, 1984,74 : 134 - 140.
  • 5Petrick JS. Monomethylarsonous acid ( MMA (Ⅲ) ) is more toxic than arsenite in Chang human Hepatocytes[J]. Toxicol Appl Pharmacol,2000,163:203-207.
  • 6Mass MJ. Methylated arsenic(Ⅲ) species react directly with DNA and are potential proximate or ultimate genotoxic forms of arsenic [ J ]. Toxicologist, 2001,14 ( 4 ) : 355- 361.
  • 7Kligerman AD, Doerr CL, Tennant AH, et al. Methylated trivalent arsenicals as candidate ultimate genotoxic forms of arsenic: induction of chromosomal mutations but not gene mutations[ J]. Environ Mol Mutagen. , 2003,42 ( 3 ) : 192-205.
  • 8Kircelli F, Akay C, Gazitt Y. Arsenic trioxide induces p53 -dependent apoptotic signals in myeloma cells with SiRNA - silenced p53 : MAP kinase pathway is preferentially activated in cells expressing inactivated p53 [J]. Int J Oncol, 2007.30(4):993 - 1001.
  • 9Zhou C, Boggess JF, Bae -Jump V, Gehrig PA. Induction of apoptosis and inhibition of telomerase activity by arsenic trioxide ( As(2 ) O ( 3 ) ) in endometrial carcinoma cells [ J ]. Gynecol Oncol, 2007,105 ( 1 ) :218-222.

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