Toxicogenomics studies reveal common and specific pathways in pulmonary, hepatic, and neuronal cell models. [SH-SY5H]. Toxicogenomics studies reveal common and specific pathways in pulmonary, hepatic, and neuronal cell models. [SH-SY5H]

To unravel possible mechanisms of Cd tissue-specificity, and to further deepen the understanding of cadmium mechanisms, we have compared transcriptomics data from cell models representative of three major Cd targets: pulmonary (A549), hepatic (HepG2), and neuronal (SH-SY-5Y) cells. Results from KEGG analysis show that only one specific pathway is dysregulated in a significant way in all cell models: the mineral absorption pathway. Overall design: Human neuroblastoma cells (SH-SY5Y) were exposed to non-cytotoxic cadmium concentrations (CdCl2) 10 or 20 µM for 24h. Two biological replicates of controls (cells grown in complete culture medium) were performd and 3 biologial replicates for each cadmium concentration used.

为解析镉（Cadmium，Cd）组织特异性作用的潜在机制，并进一步深化对镉相关作用机制的认知，本研究对比了三类代表性镉作用靶点细胞模型的转录组学（transcriptomics）数据，分别为肺源细胞系A549、肝源细胞系HepG2以及神经源细胞系SH-SY5Y。KEGG（Kyoto Encyclopedia of Genes and Genomes）分析结果显示，仅一条特异性通路在所有三类细胞模型中均出现显著失调：矿物质吸收通路。
实验整体设计：将人类神经母细胞瘤细胞SH-SY5Y暴露于浓度为10 μM或20 μM的非细胞毒性氯化镉（CdCl₂）环境中，处理时长为24小时。对照组（采用完全培养基培养的细胞）设置2次生物学重复，每一种氯化镉处理浓度均设置3次生物学重复。