AngII infusion caused two-fold increase in ROS production of WT hearts (p<0.05) (but not p47 phox KO mice), which was inhibited significantly by diphenyleneiodonium (DPI, a flavoprotein inhibitor) or superoxide dismutase, significantly but slightly by NG-nitro-l-arginine methyl ester (L-NAME, a nitric oxide synthase inhibitor), but not by rotenone (mitochondrial respiratory chain inhibitor) or oxypurinol (xanthine oxidase inhibitor). Increased ROS production in WT AngII-infused hearts was accompanied by significant phosphorylation of ERK1/2. In conclusion, p47 phox and p47 phox signalling through ERK1/2 play an important role in AngII-induced cardiac hypertrophy. Introduction Hyperglycemia-induced ROS generation within mitochondria plays a major role in the development of diabetic complications. Mitochondria are one of the most important cell organelles in diabetes research because of its crucial role as a regulator of energy balance. The present study was aimed to evaluate the effect galangin, a flavonoid, on oxidative mitochondrial damage in in streptozotocin (STZ)-induced diabetic rats. Materials and methods Diabetes was induced by intraperitoneal administration of low dose of STZ (40 mg/kg body weight (BW)) into male albino Wistar rats. Galangin (8 mg/kg BW) or glibenclamide (600 mg/kg BW) was given orally daily once for 45 days to normal and STZ-induced diabetic rats. Results Diabetic rats showed a significant (p<0.05) increase in kidney and heart mitochondrial oxidant (Thiobarbituric acid reactive substance) levels and a significant decrease in enzymatic (superoxide dismutase, glutathione peroxidase) and nonenzymatic (reduced glutathione) antioxidants levels as compared to control rats. The activities of mitochondrial enzymes such as isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, and malate dehydrogenase and mitochondrial respiratory chain enzymes such as NADH dehydrogenase and Cytochrome c-oxidase were decreased significantly (p<0.05) in diabetic rats as compared to control rats. Administration of galangin to diabetic rats resulted in the following findings as compared to diabetic control rats: the oxidant levels decreased significantly (p<0.05); the enzymatic and non-enzymatic antioxidants levels increased significantly (p<0.05); and the function of mitochondrial enzymes and the mitochondrial respiratory chain enzymes increased significantly (p<0.05).Conclusion From the results, we conclude that galangin could maintain kidney and heart mitochondrial function in diabetic rats.