• Xi Yang, Wenbin Dong, Qingping Li, Lan Kang, Xiaoping Lei, Lianyu Zhang, Youying Lu, and Xuesong Zhai.
• Department of Neonatology, Affiliated Hospital, Sichuan Medical University, Luzhou 646000, China.
• Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2015 Dec 1; 31 (12): 1669-72, 1676.

ObjectiveTo explore the relationship between deacetylase sirtuin 1 (SIRT1) and reactive oxygen species (ROS) after oxygen therapy in the peripheral blood mononuclear cells (PBMCs) of the premature infants.MethodsAccording to the fraction of inspired O2 (FiO2), premature infants diagnosed with respiratory distress syndrome (RDS) (gestational age <32 weeks), were divided into three groups: low dosage oxygen group (FiO2 <300 mL/L), moderate dosage oxygen group (FiO2; 300 mL/L-400 mL/L), high dosage oxygen group (FiO2 >400 mL/L). After 48 hours of oxygen treatment, PBMCs and serum were collected from the peripheral blood. Then the intracellular ROS level was detected by MitoSOX(TM) Red labeling combined with confocal laser scanning microscopy; the malondialdehyde (MDA) content in the serum was determined by the whole spectrum spectrophotometer; the SIRT1 localization was observed by immunofluorescence staining; and the SIRT1 levels in PBMCs were examined by Western blotting.ResultsWith the increase of FiO2, the ROS, MDA content and the rate of SIRT1 nucleocytoplasmic shuttling of PBMCs gradually increased and SIRT1 protein expression was significantly lowered.ConclusionHyperoxia induces ROS production in premature infants, promotes SIRT1 to cross from nucleus to cytoplasm, inhibits the resistant ability of SIRT1 to oxidative stress.

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