长期摄入氯化镉对金属硫蛋白和锌转运体基因转录活性的影响

A.A. Gizatullina, Yana V. Valova, D. A. Smolyankin, N. Khusnutdinova, D. Karimov, D. D. Karimov, G. F. Mukhammadiyeva, E. F. Repina
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Animals from four groups were injected with a solution of cadmium chloride in four different doses, respectively, individuals of the fifth group, the control group, received an equimolar volume of pure water. The objects of the study were the kidneys and livers of rats, removed after the animals were withdrawn from the experiment. Next, the activity of the Mt1A, Mt2A, Mt3A, Zip1 and Znt1 genes was analyzed in organ samples using real-time PCR. \nResults. Significant increases in the expression multiplicity of Mt1A, Mt2A and Mt3A metallothionein genes in the kidneys at different doses of the toxicant were revealed. In liver samples, a decrease in the expression of the Mt2A gene was found in the experimental group exposed to cadmium chloride at a dose \nof 0.1 mg/kg (p<0.05). 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引用次数: 0

摘要

简介氯化镉是一种含镉的无机化合物,镉是一种重金属,是当今活跃的环境污染物之一。镉中毒对实验动物器官的损害与人类相似。本研究对镉诱导的实验动物慢性中毒模型中金属硫蛋白和锌转运体基因的活性进行了研究。材料和方法实验使用了 72 只平均体重为 215 克的雌雄近交系白鼠。四组动物分别注射了四种不同剂量的氯化镉溶液,第五组(即对照组)的动物接受了等摩尔量的纯净水。研究对象是大鼠的肾脏和肝脏,在动物退出实验后取出。然后,使用实时 PCR 分析器官样本中 Mt1A、Mt2A、Mt3A、Zip1 和 Znt1 基因的活性。结果在不同剂量的毒物作用下,肾脏中 Mt1A、Mt2A 和 Mt3A 金属硫蛋白基因的表达倍率显著增加。在肝脏样本中,氯化镉剂量为 0.1 毫克/千克的实验组中 Mt2A 基因的表达量减少(p<0.05)。至于大鼠肝组织中的 Znt1 基因,与对照组相比,剂量为 0.001 毫克/千克时,其表达量减少(p<0.05),而剂量为 0.1 毫克/千克和 1 毫克/千克时,其表达量则增加(p<0.05),差异有统计学意义。按所述剂量接种毒物 6 个月后,对肾脏和肝脏中 Zip1 基因转录本水平的分析表明,各组之间没有显著的统计学差异。局限性。实验使用了唯一生物物种的实验动物。仅对四种剂量的镉盐进行了评估。结论研究结果表明,肾脏中 Mt1A、Mt2A 和 Mt3A 基因的表达水平可作为慢性毒物中毒的诊断指标。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of chronic intake of cadmium chloride on the transcriptional activity of metallothionein and zinc transporter genes
Introduction. Cadmium chloride is an inorganic compound containing cadmium, a heavy metal that is one of the active environmental pollutants today. Damage to organs in experimental animals due to cadmium poisoning is similar to that in humans. In this work, the activity of metallothionein and zinc transporters genes was studied in a chronic model of cadmium-induced poisoning in experimental animals. Materials and methods. The experiment was carried out using seventy two individuals of white inbred rats of both sexes, the average weight of which was 215 g. Animals from four groups were injected with a solution of cadmium chloride in four different doses, respectively, individuals of the fifth group, the control group, received an equimolar volume of pure water. The objects of the study were the kidneys and livers of rats, removed after the animals were withdrawn from the experiment. Next, the activity of the Mt1A, Mt2A, Mt3A, Zip1 and Znt1 genes was analyzed in organ samples using real-time PCR. Results. Significant increases in the expression multiplicity of Mt1A, Mt2A and Mt3A metallothionein genes in the kidneys at different doses of the toxicant were revealed. In liver samples, a decrease in the expression of the Mt2A gene was found in the experimental group exposed to cadmium chloride at a dose of 0.1 mg/kg (p<0.05). For the Znt1 gene in rat liver tissue, there was a statistically significant decrease in expression at a dose of 0.001 mg/kg (p<0.05) and, conversely, an increase at doses of 0.1 and 1 mg/kg (p<0.05) compared to the control group. Analysis of the level of transcripts of the Zip1 gene in the kidneys and liver after 6 months of inoculation with the toxicant in the presented doses did not reveal statistically significant differences between the groups. Limitations. Laboratory animals of the only biological species were used for the experiment. Four doses of the cadmium salt alone were evaluated. Conclusion. The results obtained allow concluding that the level of expression of the Mt1A, Mt2A and Mt3A genes in the kidneys can play the role of a diagnostic marker in chronic poisoning with the toxicant under study.
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