PMID- 28472013 OWN - NLM STAT- MEDLINE DCOM- 20180625 LR - 20180828 IS - 1540-0514 (Electronic) IS - 1073-2322 (Linking) VI - 48 IP - 5 DP - 2017 Nov TI - Reoxygenation with 100% Oxygen Following Hypoxia in Mice Causes Apoptosis. PG - 590-594 LID - 10.1097/SHK.0000000000000891 [doi] AB - After hypoxia, reoxygenation with air is the consensus treatment for full-term neonates; however, the effect of hyperoxic reoxygenation of adults is unknown. The present study was designed to investigate the effects of reoxygenation with 100% oxygen after hypoxia on inflammation and apoptosis in mice. Eight-week-old mice were either subjected to hypoxia in 8% oxygen for 30 min or air served as controls. Following hypoxia, mice underwent reoxygenation for 30 min with 21% or 100% oxygen. Tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), caspase-3 and brain derived neurotrophic factor (BDNF) mRNA study and histopathological study were performed. Reoxygenation with 100% oxygen significantly increased TNF-alpha (2.5 h after hypoxia), IL-1beta (5 h after hypoxia), caspase-3 (8 h after hypoxia) mRNA levels in the whole brain compared with 21% oxygen, and significantly decreased erythropoietin mRNA expression compared with 21% oxygen 9 h after reoxygenation. However, reoxygenation with 100% oxygen and 21% oxygen significantly decreased BDNF mRNA levels compared with control air group. There were no clear abnormal findings showing neuronal death among the three groups. Reoxygenation with 100% oxygen after hypoxia induced inflammation and apoptosis in adult mice. Therefore, these results suggest that the reoxygenation with 100% oxygen after hypoxia has harmful effects on adult brain as well as on neonatal brain. FAU - Nishimura, Yoshiro AU - Nishimura Y AD - *Department of Disaster and Emergency Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan daggerDepartment of Anaesthesia, Nishiwaki Municipal Hospital, Nishiwaki, Hyogo, Japan double daggerDepartment of Pharmacy, Tokushima University Hospital, Tokushima, Japan section signDepartment of Pharmacology, Osaka City University Graduate School of Medicine, Osaka, Japan ||Department of Pathology and Host Defense, Kagawa University, Kitagun, Kagawa, Japan paragraph signDepartment of Anaesthesia, Higashiosaka City Medical Center, Higashiosaka, Japan. FAU - Ueki, Masaaki AU - Ueki M FAU - Imanishi, Masaki AU - Imanishi M FAU - Tomita, Shuhei AU - Tomita S FAU - Ueno, Masaki AU - Ueno M FAU - Morishita, Jun AU - Morishita J FAU - Nishiyama, Takashi AU - Nishiyama T LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Shock JT - Shock (Augusta, Ga.) JID - 9421564 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Interleukin-1) RN - 0 (RNA, Messenger) RN - 0 (Tumor Necrosis Factor-alpha) RN - 0 (interleukin-1 delta) RN - 11096-26-7 (Erythropoietin) RN - EC 3.4.22.- (Caspase 3) RN - S88TT14065 (Oxygen) SB - IM MH - Animals MH - Apoptosis/genetics/physiology MH - Brain-Derived Neurotrophic Factor/metabolism MH - Caspase 3/metabolism MH - Erythropoietin/genetics/metabolism MH - Hypoxia/genetics/*metabolism MH - Interleukin-1/metabolism MH - Male MH - Mice MH - Mice, Inbred C57BL MH - Oxygen/*metabolism MH - RNA, Messenger MH - Tumor Necrosis Factor-alpha/metabolism EDAT- 2017/05/05 06:00 MHDA- 2018/06/26 06:00 CRDT- 2017/05/05 06:00 PHST- 2017/05/05 06:00 [pubmed] PHST- 2018/06/26 06:00 [medline] PHST- 2017/05/05 06:00 [entrez] AID - 10.1097/SHK.0000000000000891 [doi] PST - ppublish SO - Shock. 2017 Nov;48(5):590-594. doi: 10.1097/SHK.0000000000000891.