Gene expression profile in chronic mouse liver injury caused by long‐term exposure to CeCl3

• DOI: 10.1002/tox.21826
• Publication Date: 2012-11-09T11:47:14Z
• Authors: Jie Cheng; Min Fei; Min Fei; Xuezi Sang; Xuezi Sang; Zhe Cheng; Suxin Gui; Xiaoyang Zhao; Lei Sheng; Qingqing Sun; Renping Hu; Ling Wang; Fashui Hong
• Keywords: Inflammation; Male; 0301 basic medicine; Mice, Inbred ICR; Apoptosis; Cerium; 3. Good health; Oxidative Stress; 03 medical and health sciences; Liver; Liver Function Tests; Hepatocytes; Animals; Environmental Pollutants; Transcriptome; Biomarkers

Numerous studies have demonstrated lanthanide (Ln) accumulation in the liver, and corresponding damage; however, very little work has been done to evaluate relationship between Ln‐induced liver injury its gene expression profile mice. In this study, gene‐expressed profiles male mice induced by oral administration of CeCl 3 (2 mg/kg) via gavage for 90 consecutive days were investigated. The results showed that cerium accumulation, inflammation, hepatocyte necrosis observed. exposure significantly decreased counts white blood cells, lymphocyte, platelet, reticulocyte count (Ret) neutrophilic granulocyte percentages as well A/G ratio, whereas markedly increased activities alkaline phosphatase, lactate dehydrogenase, cholinesterase, concentrations triglycerides total cholesterol. Furthermore, microarray differential 675 known function genes involved immune/inflammation response, apoptosis, metabolic process, cell cycle, proliferation, cytoskeleton, oxidative stress, signal transduction, transcription, translation, transportation exposed livers, respectively. Specifically, significant downregulation Nt5e led overexpressed Cyp4a12a great suppression Cdkn1a resulted marked elevation Cel, Cyp7b1 caused disorders mouse after long‐term exposure. Therefore, these may be relation damages . © 2012 Wiley Periodicals, Inc. Environ Toxicol 29: 837–846, 2014.