The liver is an important organ in the transition from fetal to neonatal life. A significant component of this transition is an increase in hepatic mitochondrial oxidative capacity. Previous studies by Jacobs et al report an elevation in site I mitochondrial oxygen consumption after birth in rabbit hepatic mitochondria. This increase is blunted by 4 hours of neonatal hypoxia(10% FiO2). Site I oxygen consumption occurs when electrons enter the respiratory chain at complex I. We hypothesized that gene expression of NADH dehydrogenase subunit 2 (ND2) (a component of complex I encoded in the mitochondrial genome) and the 39 kD protein of complex I (encoded in the nuclear genome) would increase after birth and be altered by neonatal hypoxia. Rabbit pups were delivered by Csection at term into a 10% inspired O2 chamber. Pups were sacrificed and liver harvested either at birth (B0) or after maintenence for four hours of either normoxia (N4) (21% FiO2) or hypoxia (H4)(10%FiO2). To measure mRNA levels, we used RTPCR with an internal control. PCR products were quantified and standardized. mRNA levels of ND2 increased by 50% in the N4 animals compared to the B0 animals (B0=1.0, N4ND2=1.54±0.12*, N439 kD=1.35±0.11; *p < 0.05). We conclude that hepatic gene expression of ND2 of complex I increases with age in the normoxic rabbit pup. Interestingly, gene expression of ND2 and 39kD protein also increased in the H4 group when compared to the N4 animals (N4=1.0, H4ND2=1.81±0.22*, H439kD=1.53±0.06*; *p < 0.05). This result is intriguing because oxygen has been traditionally presumed to be the primary positive regulator of mitochondrial gene expression. This study suggests that other factors may also significantly alter mitochondrial gene expression. We speculate that this increased gene expression may be important upon reperfusion, and thereby leading to increased free radical production and enhance the injury associated with hypoxia.