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GSH is a primary substrate for enzymatic antioxidant functions and is capable of nonenzymatic radical scavenging.33 The reduced GSH and GPX1 can promote the production of reactive oxygen species (ROS), and the over-expression of ROS can promote the stability and expression of HIF-1.34,35 As a highly conserved transcription factor, HIF-1 can promote the over-expression of other hypoxia-related substrates during hypoxia, such as TGF-1, LOX and collagen, eventually aggravated penile fibrosis.36 Besides, HIF-1 can activate target genes and initiate apoptosis, cell death and autophagy.37,38 In this study, HIF-1 increased significantly in the BCNC group, while NAC down-regulated the over-expression

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64 Suppl 3, 2003, pp