title: Role of pigment epithelium-derived factor (PEDF) in arsenic-induced cell apoptosis of liver and brain in a rat model.
abstract: Although studies have shown that arsenic exposure can induce apoptosis in a variety of cells, the exact molecular mechanism of chronic arsenicosis remains unclear. Based on our previous study on human serum, the present study was to determine whether pigment epithelium-derived factor (PEDF) plays a role in the damage induced by chronic arsenic exposure in a rat model and to explore the possible signaling pathway involved. Thirty male Wistar rats were randomly divided into three groups and the arsenite doses administered were 0, 10, and 50 mg/L, respectively. The experiment lasted for 6 months. Our results showed that level of arsenic increased significantly in serum, liver, brain, and kidney in arsenic-exposed groups. It was indicated that PEDF protein was widely distributed in the cytoplasm of various types of cells in liver, brain, and kidney. PEDF protein level was only changed when the arsenite dose reached 50 mg/L in liver and brain, whereas it was not changed in the kidney. In order to investigate the possible mechanism of PEDF-exerted damages upon arsenite exposure, apoptosis in liver and brain was assessed. The proportion of apoptotic cells gradually increased with increasing arsenic administration. The ratio of Bax/Bcl-2 in the high arsenic group (50 mg/L) was significantly higher than that in the control group. Therefore, we thought PEDF played a role in cell apoptosis of liver and brain which induced by sodium arsenite exposure, and the results also demonstrated that Bax and Bcl-2 might be two key targets in the action of PEDF.
authors.affiliation: Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Hongqi
authors.initials: H
authors.lastname: Feng
authors.forename: Yanhui
authors.initials: Y
authors.lastname: Gao
authors.forename: Liyan
authors.initials: L
authors.lastname: Sun
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Li
authors.forename: Cheng
authors.initials: C
authors.lastname: Wang
authors.forename: Lijun
authors.initials: L
authors.lastname: Zhao
authors.forename: Xinxin
authors.initials: X
authors.lastname: Hu
authors.forename: Huixin
authors.initials: H
authors.lastname: Sun
authors.forename: Yudan
authors.initials: Y
authors.lastname: Wei
authors.forename: Dianjun
authors.initials: D
authors.lastname: Sun
mesh_terms: D000818:Animals; D017209:Apoptosis; D018053:Arsenites / Q000097:blood / Q000633:toxicity*; D015153:Blotting, Western; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D002452:Cell Count; D003593:Cytoplasm / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005136:Eye Proteins / Q000378:metabolism*; D007150:Immunohistochemistry; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D023421:Models, Animal; D009414:Nerve Growth Factors / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015843:Serpins / Q000378:metabolism*; D015398:Signal Transduction; D017670:Sodium Compounds / Q000097:blood / Q000633:toxicity*; D036401:Toxicity Tests, Chronic / Q000379:methods; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D000099174:Pigment Epithelium-Derived Factor
chemical_list: D018053:Arsenites; D005136:Eye Proteins; D009414:Nerve Growth Factors; D015843:Serpins; D017670:Sodium Compounds; D051028:bcl-2-Associated X Protein; D000099174:Pigment Epithelium-Derived Factor; C494828:Bax protein, rat; C017947:sodium arsenite