Developmental cigarette smoke exposure II: Kidney proteome profile alterations in 6 month old adult offspring

• Published in: Reproductive toxicology (Elmsford, N.Y.) N.Y.), 2016-10, Vol.65, p.425-435
• Main Authors: Neal, Rachel E., Jagadapillai, Rekha, Chen, Jing, Webb, Cynthia L., Stocke, Kendall, Gambrell, Cailtin, Greene, Robert M., Pisano, M.Michele
• Format: Article
• Language: English
• Subjects: Animals; Carbohydrate Metabolism - drug effects; CSE; Developmental cigarette smoke exposure; Female; Inhalation; Kidney; Kidney - drug effects; Kidney - metabolism; Maternal Exposure - adverse effects; Maternal-Fetal Exchange; Mice, Inbred C57BL; Mouse; Nucleic Acids - metabolism; Pregnancy; Prenatal Exposure Delayed Effects - chemically induced; Proteome; Proteome - drug effects; Tobacco; Tobacco Smoke Pollution - adverse effects
• ISSN: 0890-6238; 1873-1708
• DOI: 10.1016/j.reprotox.2016.05.008

•Developmental CSE induces impairment of carbohydrate metabolic pathway protein expression.•Oxidant scavenging pathways are impaired in adults by developmental CSE.•Decreased protein abundances within the nucleic acid metabolic pathways evident in mature CSE offspring. Cigarette smoke exposure (CSE) during gestation and early development suppresses the growth trajectory in offspring. In prior studies utilizing a mouse model of ‘active’ developmental CSE (GD1-PD21), low birth weight induced by CSE persisted throughout the neonatal period and was present at the cessation of exposure at weaning with proportionally smaller kidney mass that was accompanied by impairment of carbohydrate metabolism. In the present study, littermates of those characterized in the prior study were maintained until 6 months of age at which time the impact of developmental CSE on the abundance of proteins associated with cellular metabolism in the kidney was examined. Kidney protein abundances were examined by 2D-SDS-PAGE based proteome profiling with statistical analysis by Partial Least Squares-Discriminant Analysis. Key findings of this study include a persistence of impact of developmental CSE past the original exposure period on the nucleic acid and carbohydrate metabolism networks and oxidant scavenging pathways.