Hepatic oxidative injury: role of mitochondrial dysfunction in necrotizing enterocolitis

Purpose Necrotizing enterocolitis (NEC) is a severe neonatal gastrointestinal disease that can cause damage to remote organs. Previous studies have shown that inflammatory and oxidative injury occur in the liver during NEC. Mitochondrial DNA (mtDNA) plays an important role in hepatic injuries of many other diseases. We aimed to investigate the mechanism of mitochondrial dysfunction in hepatic oxidative injury during NEC. Methods NEC was induced in C57BL/6 mice (approval: 44032) by hypoxia, gavage feeding with hyperosmolar formula, and lipopolysaccharide administration from postnatal days 5 to 9 ( n = 15). Two additional groups with hypoxia only ( n = 10) and hypoxia and hyperosmolar formula ( n = 13) were also examined. Breastfed pups were used as control ( n = 15). Liver was harvested on postnatal day 9. Gene expressions of mtDNA markers cytochrome c oxidase subunit 3 ( COX3 ), cytochrome b ( CYTB ) and NADH-ubiquinone oxidoreductase chain 1 ( ND1 ) were measured by real-time qPCR. Mitochondrial morphology marker HSP60 and oxidative stress marker NRF2 were detected by immunofluorescence staining and compared between NEC and control. Data were presented as mean ± SD and compared using Student’s t test; p