目的 Obstructive sleep apnea (OSA) has been recently associated with tumor incidence and cancer-related mortality.Intermittent hypoxia (IH) mimicking OSA contributes to tumor growth and metastasis in a mouse model.Recently, the study in our lab has found that oxidative stress and inflammatory responses could mediate IH-induced melanoma lung metastasis in a mouse model of OSA (Li et al, unpublished data).Here we blocked oxidative stess with antioxidant tempol to explore the tumor lung metastasis induced by OSA-like IH.方法 C57BL/6J male mice (8-week-old) were injected with B16F10 melanoma cells via tail vein.Then these animals were randomly divided into three groups (n = 8 each)：nomoxia group, OSA-like IH group,and tempol group (exposed to IH and treated with tempol).Number of lung metastatic colonies was assessed at 21 days after exposure to IH.Lung tissues were harvested to detect the markers for oxidative stress(NF-E2-related factor 2, NRF2) and inflammation (nuclear factor kappa B P65, NF-κB P65) by western blotting.结果 The number of melanoma lung metastasis in OSA-like IH group was significantly higher than that in nomoxia group.However, this number in tempol group was significantly lower than that in IH group.The protein levels of NRF2 and NF-κB P65 in OSA-like IH group were significantly higher than that in nomoxia group.However, these levels in tempol group was significantly lower than that in IH group.结论 These results suggest that antioxidant tempol is, at least partially, capable of blocking tumor metastasis to the lung induced by OSA-like IH.Antioxidant intervention may be useful as the feasible strategy to reduce the impact of OSA on cancer modulation.