Early-Life Exposure to Cadmium Triggers Distinct Zn-Dependent Protein Expression Patterns and Impairs Brain Development

摘要: The objective of this study was to determine if the brain development impairment induced by early-life exposure cadmium (Cd) could result from changes in expression pattern distinct zinc (Zn)-dependent proteins. For purpose, adult female rats receiving either tap water, Cd, Zn, or Cd + Zn their drinking water during gestation and lactation periods were used. After birth, male offspring screened for locomotors sensorial defects. At postnatal day 21 (PND 21), pups sacrificed brains, liver, plasma taken chemical, biochemical, molecular analyses. Our results show that significantly increased metal accumulation decreased concentrations Cd-treated mothers. Besides, reduced locomotor activity open-field test, body weight, cranio-caudal length at PND21. Insulin-like growth factor-I (IGF-1) levels liver also Cd-induced disruption accompanied a significant increase superoxide dismutase (SOD) activity, induction metallothionein (MT) synthesis, and, level, an upregulation Zrt-,Irt-related protein 6 (ZIP6) gene downregulation transporter 3 (ZnT3) brain-derived neurotrophic factor (BDNF) genes brain. No on encoding other Zn-dependent proteins factors such as ZnT1, ZIP12, NF-κB, Zif268. Interestingly, supplementation provided total partial correction exposure. These data indicated ZnT3 ZIP6 well alteration transcription factors, BDNF, proteins, SOD MTs, response might be underlying mechanism impairment.