Abstract

Cadmium (Cd) is a highly toxic heavy metal that can cause severe liver damage in both humans and animals. However, the specific genes responsible for Cd-induced hepatotoxicity are still not fully understood. Therefore, the aim of this study was to identify the key genes associated with Cd-induced liver damage. To achieve this, we utilized the GSE19662 dataset from the Gene Expression Omnibus (GEO), which consisted of rat hepatocyte samples treated with cadmium chloride (CdCl2) as well as control groups. By focusing on rat hepatocytes treated with 0.10 ppm of CdCl2, the study identified 851 differentially expressed genes (DEGs), with 438 genes being upregulated and 413 genes being downregulated. Gene Ontology (GO) analysis revealed that these DEGs were primarily involved in inflammatory responses, xenobiotic metabolic processes, and the response to drugs and xenobiotic stimuli. Finally, the study identified several hub genes, including CYP2E1, CYP3A62, CYP2C11, CYP2C13, CYP2B3, HSP90B1, HSP90AA1, GSTA2, and MAPK8, which were associated with CdCl2-induced liver damage. Furthermore, pathway analysis demonstrated that these hub genes were mainly linked to pathways involved in chemical carcinogenesis, metabolic processes, steroid hormone biosynthesis, retinol metabolism, linoleic acid metabolism, arachidonic acid metabolism, inflammatory mediator regulation, Ras, and protein processing in the endoplasmic reticulum. In conclusion, this study provides important insights into the molecular mechanisms underlying Cd-induced liver damage.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call