Mitochondria are dynamic cellular organelles with Janus-faced functions that can be beneficial or deleterious to cells. Mounting evidences indicate the involvement of mitochondria dysfunction in an early stage of neurodegeneration. Parkinson’s disease (PD) is the debilitating neurodegenerative disorder that causes severe motor function impairment. Accumulating body of evidence suggests the mitochondrial dysfunction in the pathogenesis of PD. Genetic mutations in parkin have been reported in large numbers of families. In this study, we used parkin null mice model to examine the effect of parkin deficiency on mitochondrial function at basal state. Brain mitochondria were isolated from brain of young (8-10 weeks old) parkin null mice as well as wildtype littermate mice and mitochondrial respiration rates were measured as a biochemical marker of bioenergetics. Only a slight reduction in respiration rate was observed in parkin null mice compared with wildtype mice, suggesting that parkin deficiency-associated mitochondrial dysfunction at the basal state was not initiated at this young age. Evaluation at different time points should be carried out for further study.