On the contrary, in the presence of catalase suppressing the mild oxidation induced by EGCG, both SC236 and SC560 negatively affected the residual production of PGI2 with similar potency and efficacy, suggesting that COX-1 becomes the main isoform responsible for endothelial PGI2 production only under conditions of increased hydroperoxide availability such as with EGCG or, pathophysiologically, in the presence of increased oxidative stress such as in diabetes or in the presence of activated platelets. This evidence concerns the gene CAT and diabetes mellitus.