Open AccessDi‐(2‐ethylhexyl) Phthalate Upregulates ATF3 Expression and Suppresses Apoptosis in Mouse Genital Tubercle
Author(s) -
Liu Xing,
Zhang DeYing,
Li YaSha,
Xiong Jing,
He DaWei,
Lin Tao,
Li XuLiang,
Wei GuangHui
Publication year - 2009
Publication title -
journal of occupational health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 59
ISSN - 1348-9585
DOI - 10.1539/joh.l8091
Subject(s) - apoptosis , tunel assay , phthalate , western blot , terminal deoxynucleotidyl transferase , atf3 , andrology , microbiology and biotechnology , fetus , chemistry , biology , gene , medicine , gene expression , pregnancy , promoter , genetics , biochemistry , organic chemistry
Di‐(2‐ethylhexyl) Phthalate Upregulates ATF3 Expression and Suppresses Apoptosis in Mouse Genital Tubercle: Xing L iu , et al . Department of Pediatric Urology, Chongqing Children's Hospital, Chongqing Medical University, ChinaObjectives To investigate the effect of di‐(2‐ethylhexyl) phthalate (DEHP) on the expression of activating transcription factor 3 (ATF3) and apoptosis of fetal mouse genital tubercle (GT). Methods In this developmental toxicity study, pregnant C57BL/6 mice were exposed to corn oil or DEHP (100 or 500 mg/kg/ day) from embryonic day 12 (ED12) to ED16. Apoptosis was characterized by Terminal transferase dUTP nick end labeling (TUNEL) assay. Using RT‐PCR and western blot, the expressions of ATF3 and apoptosis‐related genes (P53, Bcl‐2 and Bax) were investigated. Results Apoptosis of fetal mouse GT cells notably decreased after DEHP treatment. DEHP activated ATF3 both at the mRNA and protein levels in GT. Furthermore, pro‐apoptotic P53 was down‐regulated and the ratio of anti‐apoptotic (Bcl‐2)/pro‐apoptotic (Bax) was not significantly changed. Conclusions These results suggest that DEHP may induce external genital defects via a mechanism involving apoptosis, which might correlate with the regulation of ATF3 and P53 expressions.