冯玉杰, 王玉峰, 王国琛, 李俊, 徐德祥, 王华. 急性和亚急性铅染毒后小鼠体内铅分布特征[J]. 环境与职业医学, 2018, 35(9): 849-854. DOI: 10.13213/j.cnki.jeom.2018.18209
引用本文: 冯玉杰, 王玉峰, 王国琛, 李俊, 徐德祥, 王华. 急性和亚急性铅染毒后小鼠体内铅分布特征[J]. 环境与职业医学, 2018, 35(9): 849-854. DOI: 10.13213/j.cnki.jeom.2018.18209
FENG Yu-jie, WANG Yu-feng, WANG Guo-chen, LI Jun, XU De-xiang, WANG Hua. Lead distribution characteristics in mice after acute and subacute exposures to lead[J]. Journal of Environmental and Occupational Medicine, 2018, 35(9): 849-854. DOI: 10.13213/j.cnki.jeom.2018.18209
Citation: FENG Yu-jie, WANG Yu-feng, WANG Guo-chen, LI Jun, XU De-xiang, WANG Hua. Lead distribution characteristics in mice after acute and subacute exposures to lead[J]. Journal of Environmental and Occupational Medicine, 2018, 35(9): 849-854. DOI: 10.13213/j.cnki.jeom.2018.18209

急性和亚急性铅染毒后小鼠体内铅分布特征

Lead distribution characteristics in mice after acute and subacute exposures to lead

  • 摘要: 目的 探讨急性和亚急性染毒不同剂量醋酸铅对小鼠体内铅分布的影响。

    方法 本研究包括急性和亚急性铅染毒实验。急性实验:将15只ICR雄性小鼠随机分为对照组、低铅组和高铅组,每组5只。低铅组、高铅组小鼠分别经腹腔单次给予醋酸铅溶液(25和100 mg/kg),对照组给予等容积生理盐水,染毒24 h后处死并收集生物样本。亚急性实验:将30只ICR雄性小鼠随机分为对照组(反渗透水)、低铅组(250 mg/L醋酸铅溶液)和高铅组(2 500 mg/L醋酸铅溶液),每组10只。经饮水染毒28 d后处死并收集生物样本。两项实验均收集小鼠血清、血细胞、睾丸、心脏、肝脏、肺、肾和大脑,称量脏器重量,离心收集血清,并把所有样品液氮速冻后放入-80℃冰箱保存待用。用石墨炉原子吸收分光光度计检测样品铅含量。用方差分析、秩和检验进行统计学分析。

    结果 急性铅染毒实验结果显示,与对照组相比,低剂量和高剂量铅处理明显升高小鼠血清(7.7、32.2倍)、血细胞(4.4、7.0倍)、肺脏(21.8、43.3倍)、肝脏(75.0、230.2倍)、肾脏(14.3、40.3倍)和睾丸(13.0、20.3倍)铅含量(P < 0.05);高剂量铅处理还进一步升高小鼠心脏铅含量(0.9倍,P < 0.05),但高剂量铅处理未引起大脑铅含量改变(P>0.05);不同剂量铅处理未引起小鼠体重改变(P>0.05);仅低剂量铅处理引起肺体比下降(P < 0.05)。亚急性铅染毒实验结果表明,与对照组相比,经饮水暴露低剂量和高剂量铅升高小鼠肺脏(1.7、3.0倍)、肝脏(51.4、107.5倍)、肾脏(4.7、19.7倍)和大脑(1.9、7.2倍)铅含量(P < 0.05);高剂量铅染毒还升高小鼠血清(0.4倍)、血细胞(5.3倍)、心脏(2.3倍)和睾丸(2.0倍)组织中铅含量(P < 0.05),引起小鼠饮水量下降(P < 0.05),但对小鼠体重和进食量均无影响(P>0.05);低剂量铅染毒升高心脏脏体比(P < 0.05),而高剂量铅染毒却降低肝脏脏体比(P < 0.05)。

    结论 在本实验研究条件下,急性和亚急性铅染毒均引起小鼠肺脏、肝脏和肾脏铅蓄积,且急性铅处理还引起小鼠睾丸铅蓄积,亚急性铅染毒还引起大脑铅蓄积。

     

    Abstract: Objective To investigate the effects of acute and subacute exposures to different doses of lead acetate on lead distribution in mice.

    Methods This study included acute and subacute lead exposure experiments. As for the acute lead exposure experiment, fifteen male ICR mice were randomly divided into control group, low-lead group, and high-lead group, with five mice in each group. The low-lead group and the high-lead group were given lead acetate solution (25 and 100 mg/kg) through intraperitoneal injection, while the control group was injected with equal volume of normal saline. All mice were sacrificed to collect samples at 24 h after exposure. As for the subacute lead exposure experiment, thirty male ICR mice were randomized into control group (reverse osmosis water), low-lead group (250 mg/L lead acetate solution), and high-lead group (2 500 mg/L lead acetate solution), with 10 mice in each group. Samples were collected after the mice were exposed to lead through drinking water for 28 d. For the two experiments, samples of serum, blood cells, testis, heart, liver, lung, kidney, and brain were collected from mice, and organ weights were measured. All samples were fast frozen in liquid nitrogen and stored in a -80℃ refrigerator for later detection. Graphite furnace atomic absorption spectrophotometry was used to measure lead concentration in all samples. Analysis of variance and rank test were used to analyze the experimental data.

    Results The results from the acute lead exposure experiment showed that the low-dose and the high-dose lead treatment significantly increased lead levels in serum (by 7.7 and 32.2 times), blood cells (by 4.4 and 7.0 times), lung (by 21.8 and 43.3 times), liver (by 75.0 and 230.2 times), kidney (by 14.3 and 40.3 times), and testis (by 13.0 and 20.3 times) of mice as compared to the controls, respectively (P < 0.05). The high-dose lead treatment further increased lead levels in heart (by 0.9 times, P < 0.05) of mice, but did not cause obvious changes in lead levels in brain (P>0.05). Different doses of lead treatment did not result in body weight changes in the mice (P>0.05). Only the low-dose lead treatment caused a decrease in the ratio of lung to body weight (P < 0.05). The results from the subacute lead exposure experiment showed that the lead levels in lung (by 1.7 and 3.0 times), liver (by 51.4 and 107.5 times), kidney (by 4.7 and 19.7 times), and brain (by 1.9 and 7.2 times) of mice was increased by low-dose and high-dose lead exposure via drinking water as compared to the controls, respectively. The high-dose lead exposure also significantly elevated the levels of lead in serum (by 0.4 times), blood cells (by 5.3 times), heart (by 2.3 times), and testis (by 2.0 times) of mice, reduced the drinking water consumption of mice (P < 0.05), but had no effect on body weight and diet intake. The low-dose lead exposure increased the ratio of heart to body weight (P < 0.05), whereas the high-dose lead exposure reduced the ratio of liver to body weight (P < 0.05).

    Conclusion Under the experimental conditions, both acute and subacute lead exposures cause accumulation of lead in lung, liver, and kidney of mice. Moreover, acute lead treatment induces lead accumulation in mouse testes, and subacute lead exposure results in lead accumulation in mouse brain.

     

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