Impact of maternal cigarette smoke exposure on brain inflammation and oxidative stress in male mice offspring

• DOI: 10.1038/srep25881
• Publication Date: 2016-05-12T09:17:36Z
• Authors: Yik Lung Chan; Sonia Saad; Carol Pollock; Brian Oliver; Ibrahim Al-Odat; Amgad A. Zaky; Nicole Jones; Hui Chen
• Keywords: Nitrotyrosine

Abstract Maternal cigarette smoke exposure (SE) during gestation can cause lifelong adverse effects in the offspring’s brain. Several factors may contribute including inflammation, oxidative stress and hypoxia, whose changes developing brain are unknown. Female Balb/c mice were exposed to prior mating, lactation. Male offspring studied at postnatal day (P) 1, P20 13 weeks (W13). SE dams had reduced inflammatory mediators (IL-1β, IL-6 toll like receptor (TLR)4 mRNA), antioxidant (manganese superoxide dismutase (MnSOD)) increased mitochondrial activities (OXPHOS-I, III V) protein damage marker nitrotyrosine. Brain hypoxia-inducible factor (HIF)1α its upstream signalling molecule early growth response (EGR)1 not changed dams. In offspring, IL-1R, TLR4 mRNA W13. The translocase of outer membrane MnSOD W13 with higher nitrotyrosine staining. HIF-1α was also W13, although EGR1 only P1. conclusion, maternal markers hypoxia dysfunction cell both upregulated which render their vulnerable additional insults.