Date of Award
2016
Degree Type
Thesis
Degree Name
Master of Science (MS)
First Advisor
Qian Chen, PhD, Chair
Second Advisor
Cathy J Hatcher, PhD
Third Advisor
Charlotte Greene, PhD
Fourth Advisor
Marcus Bell, PhD
Abstract
Hyperglycemia has been associated with vascular endothelial dysfunction in part by a reduction in nitric oxide (NO) production and increased oxidative stress (e.g., increased superoxide (SO) and hydrogen peroxide (H2O2). Endothelial-derived NO can be significantly reduced by increased SO/H2O2 in part by the activation of NADPH oxidase during hyperglycemia. Of the 7 NADPH oxidase isoforms, NADPH oxidase isoform 1 (NOX1) is mainly expressed in the vasculature and may play a major role in hyperglycemia induced oxidative stress and vascular endothelial dysfunction. This hypothesis was tested by measuring blood NO and H2O2 levels in real time via NO and H2O2 microsensors inserted into femoral veins of rats. Hyperglycemia (e.g., 200 mg/dl) was maintained by an i.v. infusion of 30% glucose solution for 3 hours with or without a selective NOX1 inhibitor, ML171. Hyperglycemia for 3 hours resulted in significantly higher blood H2O2 levels (3.06±0.4 μM, n=9) compared to the saline infused control (P2O2 levels by 1.86±0.61 μM (P
Recommended Citation
Mawhinney, Ashley, "Effects of NOX-1 Inhibition on Real-Time Blood Nitric Oxide and Hydrogen Peroxide in Acute Hyperglycemia" (2016). PCOM Biomedical Studies Student Scholarship. 122.
https://digitalcommons.pcom.edu/biomed/122
Included in
Chemical Actions and Uses Commons, Endocrine System Diseases Commons, Endocrinology, Diabetes, and Metabolism Commons, Nutritional and Metabolic Diseases Commons, Organic Chemicals Commons, Physiological Processes Commons