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Introduction: Several reports demonstrated that cadmium (Cd) had proinflammatory activities. The present study aimed to investigate whether Cd induces inflammatory cytokines in mouse placenta and human trophoblast cells.Methods: Human JEG-3 cells were treated with different concentration of CdCl2 (0-50 μM) or CdCl2 (25 μM) for different times. The pregnant mice were administered with CdCl2 (3.0 mg/kg, i.p.) on GD15.Results: TNF-α, IL-8 and IL-6 mRNAs were elevated in CdCl2-treated JEG-3 cells. Several inflammatory cytokines were up-regulated in Cd-treated placenta of mice. Moreover, keratinocyte chemokine (KC), a functional analogue of human IL-8, was increased in maternal serum and amniotic fluid from CdCl2-exposed mice. Additional experiment showed that gestational Cd exposure activated Akt signaling in mouse placenta. Co-culture with CdCl2 elevated pAkt level in JEG-3 cells in concentration- and time-dependent manners. LY294002, a specific inhibitor of PI3K, blocked CdCl2-evoked Akt phosphorylation in JEG-3 cells. Concomitantly, LY294002 inhibited CdCl2-induced IL-8 in JEG-3 cells. N-acetylcysteine (NAC), an antioxidant and a glutathione precursor, blocked CdCl2-evoked Akt phosphorylation in mouse placenta and human trophoblast cells. Additionally, NAC attenuated Cd-induced up-regulation of KC in amniotic fluid.Discussion: Cd induces inflammatory cytokines partially through activating Akt signaling in mouse placenta and human trophoblast cells. NAC may be exploited for prevention of Cd-induced placental inflammation. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) was a developmental toxicant that induces fetal malformation and growth restriction in mice. However, epidemiological studies about the association of maternal serum Cd level with risk of preterm birth were limited. This study was to investigate whether maternal serum Cd level during pregnancy is associated with risk of preterm birth in a Chinese population. Total 3254 eligible mother-and-singleton-offspring pairs were recruited. Maternal serum Cd level was measured by GFAAS. Based on tertiles, maternal serum Cd concentration was classified as low (L Cd, <0.65 μg/L), medium (M Cd, 0.65–0.94 μg/L) and high (H Cd, ≥0.95 μg/L). Odds ratio ( OR ) for preterm birth was estimated using multiple logistic regression models. Results showed the rate of preterm birth among L Cd, M-Cd and H Cd was 3.5%, 3.8%, and 9.4%, respectively. Subjects with H Cd had a significantly higher risk for preterm birth ( OR : 2.86; 95% CI : 1.95, 4.19; P < 0.001) than did those with L Cd. Adjusted OR for preterm birth was 3.02 (95% CI : 2.02, 4.50; P < 0.001) among subjects with H Cd compared to subjects with L Cd. Taken together, the above results suggest that maternal serum Cd level during pregnancy is positively associated with risk of preterm birth. [ABSTRACT FROM AUTHOR]