The effects of lead exposure on placental NF-kappaB expression and the consequences for gestation.
The present study was designed to investigate the toxicity of lead exposure on the placenta at different dosages and the relationship with placental expression of NF-kappaB. A total of 67 unrelated Han Chinese pregnant women and 108 Wistar rats were included in this study. The rats were randomly divided into four groups for consumption of water with or without 0.025% lead acetate during various gestational periods; blood samples and placenta were harvested for analysis. Blood lead content was determined by atomic absorption spectrophotometry. Placental NF-kappaB expression was evaluated by immunohistochemistry. Placental cytoarchitecture was examined by histopathology and electronic microscopy. Fetal body weight, body length and placental weight was significantly lower (p<0.05) in the lead-exposed rats compared to controls. Maternal blood lead levels in the rats negatively correlated with placental weight (r=0.652, p<0.01). Rat placenta showed focal necrosis in the decidua with trophoblast degeneration and fibrin deposition. Mitochondria were swollen and decreased in number, rough endoplasmic reticula were distended and ribosomal number on membranes decreased. In the human placenta, we did not find abnormal cytoarchitecture. On the other hand, placental expression of NF-kappaB in lead-exposed rats was significantly higher than that in controls and the expression of NF-kappaB in human placenta was positively correlated with maternal blood lead levels (r=0.663, p<0.01). These findings suggest that lead exposure at various gestational periods produce varied effects, with NF-kappaB activation following lead exposure. Injury to cytoplasmic organelles may interfere with the nutrition and oxygen exchange between mother and fetus, which may be contribute to abnormal pregnancy outcomes.
Wang
Yun-ying
YY
Department of Medical Genetics, Affiliated Qingdao Municipal Hospital of Qingdao University Medical College, Qingdao, Shandong 266011, People's Republic of China.
Sui
Ke-xu
KX
Li
Hong
H
Ma
Hai-yan
HY
D000328:Adult; D000818:Animals; D018568:Crown-Rump Length; D004305:Dose-Response Relationship, Drug; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D020567:Fetal Weight / Q000187:drug effects; D005865:Gestational Age; D006801:Humans; D007854:Lead / Q000009:adverse effects* / Q000097:blood; D008297:Male; D008431:Maternal-Fetal Exchange; D016328:NF-kappa B / Q000378:metabolism*; D009929:Organ Size / Q000187:drug effects; D009942:Organometallic Compounds / Q000097:blood / Q000633:toxicity*; D010920:Placenta / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D018570:Risk Assessment; D055815:Young Adult
D016328:NF-kappa B; D009942:Organometallic Compounds; D007854:Lead; C008261:lead acetate