Anhui Key Laboratory of Poultry Infectious Disease Prevention and Control, College of Animal Science, Anhui Science and Technology University, Fengyang, 233100, China.
Biological Applications Department, Nuclear Research Center, Egyptian Atomic Energy Authority, Abu-Zaabal, 13759, Egypt.
Biol Trace Elem Res. 2023 Apr;201(4):1913-1934. doi: 10.1007/s12011-022-03294-4. Epub 2022 Jun 2.
Chromium exposure has adverse impacts on human health and the environment, whereas chromate-induced hepatotoxicity's detailed mechanism is still unclear. Therefore, the purpose of the current study was to reveal the crucial signaling pathways and genes linked to sodium chromate-induced hepatotoxicity. GSE19662, a gene expression microarray, was obtained from Gene Expression Omnibus (GEO). Six primary rat hepatocyte (PRH) samples from GSE19662 include sodium chromate-treated (n = 3) and the control PRH samples (n = 3). A total of 2,525 differentially expressed genes (DEGs) were obtained, especially 962, and 1,563 genes were up- and downregulated in sodium chromate-treated PRHs compared to the control. Gene ontology (GO) enrichment analysis suggested that those DEGs were involved in multiple biological processes, including the response to toxic substances, the positive regulation of apoptotic process, lipid and cholesterol metabolic process, and others. Signaling pathway enrichment analysis indicated that the DEGs were mainly enriched in MAPK, PI3K-Akt, PPAR, AMPK, cellular senescence, hepatitis B, fatty acid biosynthesis, etc. Moreover, many genes, including CYP2E1, CYP1A2, CYP2C13, CDK1, NDC80, and CCNB1, might contribute to sodium chromate-induced hepatotoxicity. Taken together, this study enhances our knowledge of the potential molecular mechanisms of sodium chromate-induced hepatotoxicity.
铬暴露对人类健康和环境有不良影响,而铬酸盐诱导的肝毒性的详细机制尚不清楚。因此,本研究的目的是揭示与铬酸钠诱导的肝毒性相关的关键信号通路和基因。GSE19662 是从基因表达综合数据库(GEO)中获得的基因表达微阵列。GSE19662 中的 6 个原代大鼠肝细胞(PRH)样本包括铬酸钠处理组(n=3)和对照组 PRH 样本(n=3)。共获得 2525 个差异表达基因(DEGs),其中铬酸钠处理组 PRH 中上调和下调的基因分别有 962 个和 1563 个。基因本体(GO)富集分析表明,这些 DEGs 参与了多种生物学过程,包括对有毒物质的反应、细胞凋亡过程的正向调节、脂质和胆固醇代谢过程等。信号通路富集分析表明,DEGs 主要富集在 MAPK、PI3K-Akt、PPAR、AMPK、细胞衰老、乙型肝炎、脂肪酸生物合成等通路中。此外,许多基因,如 CYP2E1、CYP1A2、CYP2C13、CDK1、NDC80 和 CCNB1,可能参与了铬酸钠诱导的肝毒性。总之,本研究加深了我们对铬酸钠诱导的肝毒性潜在分子机制的认识。