Sodium Arsenite Inhibits Proliferation and Induces Apoptosis of Human Hepatic Cells
10.13865/j.cnki.cjbmb.2021.09.1686
- Author:
Bao-Fei SUN
1
;
He-Ping YANG
1
;
Jia YU
2
;
Heng LUO
2
;
Bao-Fei SUN
3
;
Ai-Hua ZHANG
3
;
Heng LUO
4
Author Information
1. Department of Anatomy, School of Basic Medical Sciences, Guizhou medical university
2. State Key Laboratory f Functoions and Applications of Medicinal Plants, Guizhou Medical University
3. The Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, Department of Toxicology, School of Public Health, Guizhou Medical University
4. The Key Laboratory of Chemistry for Natural Products of Guizhou Province, Chinese Academy of Science
- Publication Type:Journal Article
- Keywords:
arsenite (SA);
DNA repair pathway;
human hepatic cells;
RecQ helicases
- From:
Chinese Journal of Biochemistry and Molecular Biology
2021;37(11):1528-1539
- CountryChina
- Language:Chinese
-
Abstract:
Arsenic is a potent toxic heavy metal found in the environment that can causes health problems, including liver disease in humans and animals. Chronic exposure to arsenic remains an environmental health problem worldwide, affecting hundreds of millions of people. Although the oxidative stress and apoptosis induced by arsenic have been confirmed, the underlying mechanism of apoptosis has not been fully elucidated. The purpose of this study is to investigate whether sodium arsenite (SA)induced liver toxicity is related to the regulation of DNA replication and repair pathways. The results of MTT and microscopy showed that SA has an inhibitory effect on the proliferation of human hepatocytes (L02), and this effect is time and concentration dependent. Flow cytometry detected the effects of different concentrations of SA on L02 cells. Compared with the control group, high concentrations of SA significantly affected the L02 cell cycle. In addition, RNA sequencing results showed that the differentially expressed genes in cells after SA treatment were concentrated in the DNA replication process and repair pathways. The effect of SA treatment on the expression of human RECQ DNA helicase and repair genes was further confirmed by Western blot and real-time quantitative PCR. In vitro study showed that SA treatment inhibited cell proliferation, and induced apoptosis as well as DNA damage and cell cycle arrest of human liver cell L02. Collectively, these results indicate that arsenic poisoning is related to the regulation of DNA replication and repair pathways, which provides insight for understanding the molecular mechanism of arsenic poisoning.
