Objective To explore the mechanism of gastrointestinal dysfunction caused by chronic renal failure (CRF), and to determine whether colon is involved in the activation of oxidative stress (OS) in CRF.Methods Thirty male SD rats were randomly divided into control group (n=10) and CRF group (n=20). The rats in the CRF group were treated with 5/6 nephrectomy to establish CRF model, and the rats in the control group were only sutured after opening renal capsule. The rats were sacrificed at 10 weeks after model administration, and the serums and colon tissues near ileocecal valve were collected. Blood urea nitrogen (BUN) and serum creatinine (SCr) were measured to evaluate the success of the model. Malonodialdehyde (MDA), superoxide dismutase (SOD), total antioxidant capacity (TAC) and 8-hydroxy deoxyguanosine (8-OHdG) in the serum and colon tissues were detected to evaluate the level of OS. The ubiquinol cytochrome C reductase core proteinⅠ(UQCRC1) was tested for the evaluation of mitochondrial function.Results Compared with the control group, the levels of BUN and SCr in serum of the rats in the CRF group were increased, suggesting that the model was successfully established. Compared with the control group, serum and colonic MDA levels were significantly increased in the CRF group (P<0.05); however, there were no significant differences in 8-OHdG or anti-oxidative markers (SOD, TAC) in serum or colon tissues between the two groups (P >0.05). The protein level of UQCRC1 in colon tissues was significantly reduced in the CRF group compared with the control group (P<0.05). However, there was no significant difference in the mRNA level of UQCRC1 in colon tissues between the control and CRF groups (P >0.05).Conclusion There is an imbalance between oxidation and antioxidation in the colonic tissues of CRF rats, which may be related to mitochondrial dysfunction.