The testis of the SCD mouse exhibits upregulation of 4-hydroxy-2-nonenal (4-HNE), a major end product of lipid peroxidation, upregulation of NOX gp91phox subunit, and uncompensated expression of the antioxidant enzyme glutathione peroxidase-1, all consistent with a heightened and uncontrolled redox environment in the SCD mouse Leydig cell (31). This evidence concerns the gene GPX1 and Schnyder corneal dystrophy.