ABSTRACT

Protective Effects of Zinc Supplementation for Diabetes-Induced Vascular Damage Diabetes 

Stephanie MacKenzie


The leading cause of mortality in diabetic patients is cardiovascular disease developed through the accumulation of damage done by oxidative stress. Hyperglycemic conditions activate pathogenic pathways, including mitochondrial dysfunction, which generate reactive oxygen species. The endogenous antioxidant defense system is unable to adequately mitigate this damage as diabetes is linked with zinc deficiency, and zinc plays a crucial role in the functionality of the antioxidant system. The effects of zinc supplementation in the prevention of diabetic cardiomyopathy have been documented in previous research. However, the protective capacity of zinc supplementation in the vasculature has yet to be established. We hypothesized that a four-week zinc supplementation intervention would enhance mitochondrial respiration, reduce protein oxidation, and increase the expression of several important antioxidants (superoxide dismutase (SOD), zinc-induced metallothionein (MT), catalase, and peroxiredoxin-2 (Prx2)) in the vasculature of streptozotocin-induced diabetic mice when compared to diabetic controls. Results revealed that mitochondrial respiration was significantly more efficient in the zinc-supplemented group. Additionally, it was found that the intervention group experienced significantly reduced levels of protein oxidation as well as a significant upregulation in both SOD and MT expression. No differences were observed among levels of catalase and Prx2. These findings suggest that zinc supplementation may have the potential to prevent deleterious changes in mitochondrial health and act in a protective capacity against oxidative damage in the vasculature.