title: Effects of lead exposure on placental cellular apoptosis and endoplasmic reticulum stress in rats.
abstract: BACKGROUND
  Lead exposure during pregnancy contributes to fetal abortion and/or teratogenesis. Endoplasmic reticulum (ER) apoptosis can be induced by various pathological conditions when ER function is disturbed. However, it is unclear whether ER stress and apoptosis play a role in the etiology of lead-exposed disease status. We aimed to investigate whether lead induced placental apoptosis and subsequent toxicity is initiated by ER apoptosis via caspase-12.
  
  
  METHODS
  Sixty-three female Wistar rats were exposed to lead in drinking water during various gestational periods. Blood lead level was determined by atomic absorption spectrophotometry. Placental cytoplasmic organelles were examined by electronic microscopy. Placental caspase-12 mRNA expression was evaluated by qRT-PCR. TUNEL assay was used to determine the placental apoptosis.
  
  
  RESULTS
  Lead exposure significant induced ER apoptosis compared to that of the controls (P < 0.05), accompanied with increased caspase-12 mRNA expression. Significant differences of caspase-12 mRNA expression levels were observed among the four groups (F = 13.78, P < 0.05). Apoptotic index (AI) was significantly increased in experimental groups compared to that of the controls (F = 96.15, P < 0.05). In lead-exposed groups, trophoblast cells underwent degeneration and fibrin deposition; Mitochondria were swollen and decreased in number; ER swelling, expansion, and vacuolization were observed.
  
  
  CONCLUSIONS
  Lead exposure contributes to placental apoptosis, as well as increased caspase-12 mRNA expression, which in turn promoted ER stress.
authors.affiliation: Department of Medical Genetics, Qingdao Municipal Hospital, Qingdao University Medical College, Qingdao, Shandong 266071, China.
authors.forename: Yunying
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Obstetrics and Gynecology, Qingdao Municipal Hospital, Qingdao University Medical College, Qingdao, Shandong 266011, China.
authors.forename: Haiyan
authors.initials: H
authors.lastname: Hu
authors.affiliation: Department of Medical Genetics, Qingdao Municipal Hospital, Qingdao University Medical College, Qingdao, Shandong 266071, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Li
authors.affiliation: Department of Medical Genetics, Qingdao Municipal Hospital, Qingdao University Medical College, Qingdao, Shandong 266071, China. Email: mahy_cn@sohu.com.
authors.forename: Haiyan
authors.initials: H
authors.lastname: Ma
authors.affiliation: Department of Obstetrics and Gynecology, Qingdao Municipal Hospital, Qingdao University Medical College, Qingdao, Shandong 266011, China.
authors.forename: Fengsen
authors.initials: F
authors.lastname: Xu
authors.affiliation: Department of Medical Genetics, Qingdao Municipal Hospital, Qingdao University Medical College, Qingdao, Shandong 266071, China.
authors.forename: Baoming
authors.initials: B
authors.lastname: Qu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects*; D005260:Female; D007854:Lead / Q000633:toxicity*; D010920:Placenta / Q000166:cytology* / Q000648:ultrastructure; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar
chemical_list: D007854:Lead