饮水途径镉暴露后小鼠体内镉分布研究

doi:10.3969/j.issn.1004-616x.2024.06.008

摘要/Abstract

摘要： 目的： 检测经饮水途径镉暴露后小鼠血液、食管、肝及肾组织中的镉蓄积浓度，为镉的毒性评价和镉与食管相关疾病关联研究提供补充依据。方法： 试验设对照组、氯化镉(CdCl₂)低剂量(10 mg/kg)和高剂量(75 mg/kg)处理组。对照组给予标准饲料和双蒸水，镉处理组给予标准饲料和含相应浓度CdCl₂溶液。对照组和低剂量镉处理组小鼠均分别暴露8、12、16和20周，高剂量组暴露16周。将27只SPF级C57BL/6小鼠按时间点分组，每组3只。通过眼眶取血收集对照组第8和12周，低剂量组第8、16和20周以及高剂量组第16周的小鼠全血；按试验分组时间节点处死小鼠，收集食管、肝、肾组织，采用电感耦合等离子质谱仪(ICP-MS)进行镉浓度检测。结果： 与对照组比较，低剂量镉处理组血镉水平显著升高(P<0.01)，但组内各暴露时间点差异无统计学意义(P>0.05)，高剂量镉处理16周组血镉水平较低剂量组显著升高(P<0.01)。食管镉浓度在低剂量镉处理组各暴露时间点均高于对照组(P<0.05或P<0.01)，且在第20周时镉含量最高(67.7 μg/L)，与第8周(44.0 μg/L)和第12周(35.2 μg/L)比较差异均具有统计学意义(P<0.05或P<0.01)。此外，高剂量镉处理16周组食管镉浓度(129.2 μg/L)显著高于低剂量组(47.9 μg/L，P<0.01)。与对照组比较，低剂量镉处理组肝、肾组织镉浓度分别在镉暴露12~16周和8~16周时显著升高(P<0.05或P<0.01)，于16周时达到峰值(P<0.01)后回落。16周时各剂量组间肝、肾镉浓度差异均有统计学意义(P<0.01)，其中高剂量处理组镉浓度最高。对照组和镉处理组小鼠血液、食管、肝脏和肾脏均能检测到镉，镉含量从高到低依次为肾脏>肝脏>食管>血液。结论： 经饮水途径镉暴露后小鼠血液、食管、肝和肾组织中的镉浓度分布各异，且与暴露时间和剂量有关。

关键词: 镉, 小鼠, 蓄积, 电感耦合等离子体质谱, 食管

Abstract: OBJECTIVE： This study aimed to elucidate the distribution，accumulation and toxicity of cadmium in the blood，esophagus，liver，and kidneys of mice following subchronic exposure of cadmium in drinking water. METHODS： For this study，27 pathogen-free (SPF)-grade C57BL/6J mice were randomly assigned to a control，low-dose (10 mg/kg CdCl₂)，and high-dose groups (75 mg/kg CdCl₂). The control group received standard feed and double-distilled water，while the exposed groups were given standard feed and a solution containing the corresponding concentration of CdCl₂. The low-dose group was exposed to cadmium for 8，12，16，and 20 weeks，and the high-dose group for 16 weeks，with three mice per time point. Whole blood was collected from the orbital cavity of mice of the control group at 8 and 12 weeks，the low-dose group at 8，16，and 20 weeks，and the high-dose group at 16 weeks. Mice were sacrificed according to the experimental time points，and esophageal，liver，and kidney tissues were collected. Cadmium levels were measured using inductively coupled plasma mass spectrometry (ICP-MS). RESULTS： Blood cadmium levels in the treated groups were significantly higher than in the control group (P<0.01). The blood cadmium levels in the low-dose group were significantly increased compared to the control (P<0.01)，but there was no statistically significant difference among the different exposure time points within the group (P>0.05). At the 16-week time point，the blood cadmium levels in the high-dose group were significantly higher than in the low-dose group (P<0.01). The esophageal cadmium concentration in the low-dose group was higher than in the control group at all exposure time points (P<0.05 or P<0.01)，with the highest concentration at 20 weeks (67.7 μg/L)，which was statistically significant compared to 8 weeks (44.0 μg/L) and 12 weeks (35.2 μg/L) (P<0.05 or P<0.01). The esophageal cadmium concentration in the high-dose group (129.2 μg/L) at 16 weeks was significantly higher than in the low-dose group (47.9 μg/L，P<0.01). In the low-dose group，cadmium concentrations in liver and kidney tissues increased from 12-16 weeks and 8-16 weeks，respectively，compared to the control group (P<0.05 or P<0.01)，reaching a peak at 16 weeks (P<0.01) before declining. At 16 weeks，there were statistically significant differences in the cadmium concentrations of liver and kidney tissues among all dose groups，with the highest concentrations in the high-dose group (P<0.01). Cadmium levels were quantifiable in the blood，esophagus，liver，and kidneys of both control and cadmium-treated groups，with the highest to lowest order of cadmium content being kidney>liver>esophagus>blood. CONCLUSION： Dietary cadmium exposure resulted in the accumulation of cadmium in the blood，esophagus，liver，and kidney of mice，exhibiting a definite time- and dose-dependent effect.

Key words: cadmium, mice, accumulation, inductively coupled plasma mass spectrometry, esophagus

中图分类号:

R994.6

何丽华, 罗嘉楠, 张厦蓉, 陈炯玉, 谢冰梦, 彭琳. 饮水途径镉暴露后小鼠体内镉分布研究[J]. 癌变·畸变·突变, 2024, 36(6): 470-475,496.

HE Lihua, LUO Jianan, ZHANG Xiarong, CHEN Jiongyu, XIE Bingmeng, PENG Lin. Distribution of cadmium in mice after exposure to cadmium via drinking water[J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2024, 36(6): 470-475,496.

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