• EXAMINING THE EFFECTS OF AETOKTHONOS HYDRILLICOLA EXTRACT ON OXIDATIVE STRESS IN C6 CELLS

      Ward, Kayla; Department of Biological Sciences; Wiley, Faith; Augusta University (2019-02-13)
      Aetokthonos hydrillicola, a species of cyanobacteria, has colonized an invasive species of hydrilla in the lakes of the Southeastern United States. This cyanobacterium is suspected to cause Avian Vacuolar Myclinopathy (AVM). AVM is a neurological disease that affect birds. Bald eagles and American coots have been primarily studied and known to be affected by AVM. Symptoms of AVM consist of brain lesions, loss of basic motor skills, and the disease often leads to death. Extracts of A. hydrillicola are toxic to C6 cells, and this cell line is used as a model to examine the mechanism of toxicity. The aim of this research project is to understand the role of oxidative stress in A. hydrillicola cytotoxicity and determine if antioxidant compounds may protect the cells. Common oxidative stress inhibitors, Gingko biloba extract and selenium, have been tested in different concentrations in order to determine if oxidative stress is present and preventable. These compounds did not prevent toxicity in the C6 cells exposed to the cyanobacterial extracts. The presence of oxidative is currently being further investigated using a 2-7 dichlorofluorescin diacetate (DCFH-DA) assay, which indicates the presence of reactive oxygen species.
    • Peroxynitrite Mediates Diabetes-Induced Endothelial Dysfunction: Possible Role of Rho Kinase Activation

      El-Remessy, Azza B.; Tawfik, Huda E.; Matragoon, Suraporn; Pillai, Bindu; Caldwell, Ruth B.; Caldwell, Robert William; Department of Pharmacology and Toxicology; Vascular Biology Center (2010-11-1)
      Endothelial dysfunction is characterized by reduced bioavailability of NO due to its inactivation to form peroxynitrite or reduced expression of eNOS. Here, we examine the causal role of peroxynitrite in mediating diabetes-induced endothelial dysfunction. Diabetes was induced by STZ-injection, and rats received the peroxynitrite decomposition catalyst (FeTTPs, 15â mg/Kg/day) for 4 weeks. Vasorelaxation to acetylcholine, oxidative-stress markers, RhoA activity, and eNOS expression were determined. Diabetic coronary arteries showed significant reduction in ACh-mediated maximal relaxation compared to controls. Diabetic vessels showed also significant increases in lipid-peroxides, nitrotyrosine, and active RhoA and 50% reduction in eNOS mRNA expression. Treatment of diabetic animals with FeTTPS blocked these effects. Studies in aortic endothelial cells show that high glucose or peroxynitrite increases the active RhoA kinase levels and decreases eNOS expression and NO levels, which were reversed with blocking peroxynitrite or Rho kinase. Together, peroxynitrite can suppress eNOS expression via activation of RhoA and hence cause vascular dysfunction.