That NAC/ALP treatment can enhance endogenous GSH/GSSG to a level higher than observed in control rats at basal may explain why chronic NAC/ALP treatment prevented the compensatory increase in myocardial Cu/Zn SOD in diabetes or even reduced cardiac Cu/Zn SOD and Mn SOD after ischemia, but still decreased cardiac and plasma 15-F2t-Isop to levels comparable to those in the control group and also reduced post-ischemic myocardial infarction in the diabetic rats. The gene discussed is SOD2; the disease is diabetes mellitus.