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Journal of Environmental Pathology, Toxicology and Oncology
IF: 1.241 5-Year IF: 1.349 SJR: 0.356 SNIP: 0.613 CiteScore™: 1.61

ISSN Print: 0731-8898
ISSN Online: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.v31.i2.20
pages 95-107

Reactive Oxygen Species Mediate Cr(VI)-induced S Phase Arrest Through p53 in Human Colon Cancer Cells

Lijuan Sun
Graduate Center for Toxicology, University of Kentucky, Lexington, Kentucky
Xin Wang
Graduate Center for Toxicology, University of Kentucky, Lexington, Kentucky
Hua Yao
Department of Stomatology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
Wenqi Li
Graduate Center for Toxicology, University of Kentucky, Lexington, Kentucky
Young-Ok Son
Graduate Center for Toxicology, University of Kentucky, Lexington, Kentucky
Jia Luo
Department of Internal Medicine, College of Medicine, University of Kentucky, Lexington, Kentucky
Jiankang Liu
Institute of Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Xi'an Jiaotong University School of Life Science and Technology, Xi'an, China
Zhuo Zhang
Toxicology and Cancer Biology, College of Medicine, University of Kentucky, Lexington, KY

ABSTRACT

Compounds that contain chromate (Cr(VI)) are well-known carcinogens that are present in both industrial settings and the environment. The mechanism of carcinogenesis associated with these compounds is not well understood. This study focused on Cr(VI)-induced cell cycle arrest in human colon adenocarcinoma DLD1 cells. Treatment of the cells with Cr(VI) at 2.5 µM caused a growth arrest at the S phase. An increase in Cr(VI) concentration enhanced the growth arrest. Superoxide dismutase did not alter the Cr(VI)-induced S phase arrest. Catalase inhibited S-cell growth, indicating that H2O2 is an important mediator in Cr(VI)-induced S phase arrest. Electron spin resonance spin-trapping measurements showed that incubation of cells with Cr(VI) generated hydroxyl radical (·OH). Catalase inhibited ·OH generation, indicating that H2O2 was generated from cells stimulated by Cr(VI) and that H2O2 functioned as a precursor of ·OH radical generation. p53, an oxidative response transcription factor, was activated upon Cr(VI) stimulation. Inhibition of p53 by introducing small hairpin RNA decreased S phase arrest induced by Cr(VI). These results support the following conclusions: (1) reactive oxygen species (ROS) are generated in Cr(VI)-stimulated DLD1 cells; (2) among the ROS generated, H2O2 played a major role in causing S phase arrest in DLD1 cells; and (3) ROS mediated S phase arrest through a p53-dependent pathway.


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