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王春, 陈刚, 仇梁林, 江俊康, 唐勇, 李晓东, 姚陈娟. 三价砷进入小鼠胃肠道生物转运途径分析[J]. 中国公共卫生, 2011, 27(4): 459-461. DOI: 10.11847/zgggws2011-27-04-35
引用本文: 王春, 陈刚, 仇梁林, 江俊康, 唐勇, 李晓东, 姚陈娟. 三价砷进入小鼠胃肠道生物转运途径分析[J]. 中国公共卫生, 2011, 27(4): 459-461. DOI: 10.11847/zgggws2011-27-04-35
WANG Chun, CHEN Gang, QIU Liang-lin, . Biotransportation of arsenite into gastrointestinal tissues in mice[J]. Chinese Journal of Public Health, 2011, 27(4): 459-461. DOI: 10.11847/zgggws2011-27-04-35
Citation: WANG Chun, CHEN Gang, QIU Liang-lin, . Biotransportation of arsenite into gastrointestinal tissues in mice[J]. Chinese Journal of Public Health, 2011, 27(4): 459-461. DOI: 10.11847/zgggws2011-27-04-35

三价砷进入小鼠胃肠道生物转运途径分析

Biotransportation of arsenite into gastrointestinal tissues in mice

  • 摘要: 目的探索三价砷进入小鼠胃肠道的生物转运途径。方法雄性小鼠分为对照组、砷染毒组(As3+10mg/kg)、汞+砷染毒组(Hg2++As3+各10 mg/kg)、甘油+砷染毒组(体积比1:1),进行灌胃染毒和原位小肠灌流实验。石墨炉原子吸收法测定各组小鼠胃肠中段组织中砷浓度,反转录-聚合酶链式反应法对胃肠组织中水-甘油通道蛋白(AQGP3、7、9)基因mRNA表达水平进行半定量检测。结果小鼠砷灌胃染毒后胃和小肠组织中砷浓度分别为(108.62±6.72)和(13.47±2.48)μg/g,胃组织中砷浓度明显高于小肠组织(P<0.01)。给予水-甘油通道蛋白抑制剂汞或甘油后再给予砷,胃组织中砷浓度分别为(72.05±7.98)、(88.57±9.34)μg/g,肠组织中砷浓度分别为(8.88±0.95)、(8.06±1.20)μg/g,均比单独染砷时明显下降(P<0.01);原位小肠灌流后汞+砷处理组及甘油+砷处理组小肠组织中砷浓度(10.37±0.29)、(10.21±0.44)μg/g比砷处理组(13.94±0.78)μg/g明显降低(P<0.01);胃肠组织中广泛表达水-甘油通道蛋白基因,胃体部AQP3表达水平与空肠比较,差异有统计学意义(P<0.05)。结论水-甘油通道蛋白可能参与三价砷在小鼠胃肠道的生物转运。

     

    Abstract: ObjectiveTo explore the route of arsenite biotransportation into gastrointestinal tissues in mice.MethodsAs(Ⅲ)of 10mg/kg was administered by gavage or in suit perfusion to male mice with or without Hg(Ⅱ)or glycerol, inhibitors of aquaglyceroporins(AQGPs).The concentrations of inorganic arsenic(iAs)in stomach body and jejunum were determined by graphite furnace atomic absorption spectrometry(GFAAS).AQGPs(AQP3,7,9)mRNA expression levels were detected by reverse transcriptase-polymerase chain reaction(RT-PCR).ResultsiAs content in stomach(108.62± 6.72μg/g)was much higher than that in intestine(13.47±2.48μg/g,P<0.01)after As(Ⅲ)administration by gavage.The concentrations of iAs were significantly decreased after administration of As(Ⅲ)with AQGPs inhibitors(P<0.01).In stomach,the levels of iAs decreased to 72.05±7.98μg/g after Hg(Ⅱ)co-administration and to 88.57±9.34μg/g after glycerol co-administration.The corresponding iAs levels in intestine were 8.88±0.95μg/g and 8.06±1.20μg/g,respectively.Similar results were obtained in the experiment of in situ perfusion.Compared with the iAs level in As(Ⅲ)treated group(13.94±0.78μg/g),the iAs levels decreased significantly in Hg(Ⅱ)+As(Ⅲ)group(10.37±0.29μg/g),as well as in glycerol+As(Ⅲ)group(10.21±0.44μg/g,P<0.01).AQP3,7,9 mRNA were extensively expressed in gastrointestinal tissues.The expression level of AQP3 mRNA in stomach body was much higher than that in jejunum (P<0.05).ConclusionArsenite may be biotransported by AQGPs into murine gastrointestinal tissues.

     

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