The E. coli ArsA is involved in arsenic detoxification but the role of yArsA (ArsA homologue of Saccharomyces cerevisiae, encoded by YDL100C ORF) in yeast is still undefined. Disruption of YDL100C ORF is not lethal. To study the role of yArsA in oxidative tolerance, wild type and knock out strain were grown in presence or absence of 1 mM H2O2 and assayed the expression of anti-oxidation machanisms . The results show that molecular oxidation is higher and catalase activity is lower in KO compared with WT. It suggests that increased ROS and decreased catalase activity are the cause of cell death. Further analysis of the expression of ROS defense mechanisms by RT-PCR show that there is no significant difference in TRR1, GSH1, and SOD1 expression in WT and KO grown in presence of 1 mM H2O2 but the CTT1, TPS1, NTH1 expression in KO are less than WT grown under oxidative stress. GSH contents is consistent with the result of RT-PCR, and trehalose contents is higher in KO strain under oxidative stress. Loss of catalase activity and decreased efficiency of degrading trehalose suggest that the deficiency in activation of general stress response in KO when grown in the presence of H2O2. Therefore, yArsA would be involved in expressing the general stress response in oxidative tolerance.

Aluminum-treated rice seeding (Oryza sativa L. cv. Taichung Native 1 and O. sativa L. cv. Tainung 67) showed significant inhibition in rice root growth, and an enhancement of POX activity. In Tainung 67 cultivar rice synthesizes more lignin in Al-treated tissue. Meanwhile, the decrease of H2O2 levels is accompanied with the enhancement of POX activity in Al-treated tissue. The increase in POX activity induced by Al might remove excess hydrogen peroxide serving a detoxifying role and synthesizing more lignin for protection. In Taichung native 1 cultivar, high amounts of H2O2 accumulated in Al-treated tissues could be due to the less amounts of POX induced by Al. In response to Al treatment, the Taichung native 1 cultivar synthesizes less lignin in comparison with that of Tainung 67, and is more Al-less tolerant. Therefore, the Tainung 67 cultivar is more tolerant to Al than Taichung native 1.

No description available.

Contraction of cardiac muscle is a highly regulated event that relies on a delicate balance of ions entering and leaving the cell through ion channels. In particular, voltage gated sodium channels are responsible for the rapid depolarization that leads to a contraction. During an oxidative challenge, sodium channels rapidly activate, but do not fully turn off. This alters the rate of cardiac repolarization and can induce cardiac arrhythmias. It is currently unknown whether the most common sodium channel isoform found in the heart, NaV1.5, generates this oxidant-induced persistent current or if other isoforms are responsible. Therefore, I sought to further explore the biophysical properties NaV1.5, and determine if it can enter this persistent mode. I tested the biophysical properties of native INa in cardiac myocytes and in NaV1.5 transfected HEK293 cells under macro cell-attached voltage-clamp. I used a sodium channel enhancer (Anemonia sulcata toxin II; 10 nM), a sodium channel blocker (tetrodotoxin; 10 nM) and a model of oxidative stress (H2O2; 100 µM, 200 µM, 1000 µM) to compare and contrast the cellular responses between both cell types. I observed that transfected HEK293 cells and cardiac myocytes were unaffected by H2O2 at various concentrations. Given the lack of other isoforms in transfected HEK293 cells, and the low abundance (<5%) of other isoforms in cardiac myocytes, I propose that NaV1.5 function is unaffected by H2O2. Furthermore, ATX II prolonged the inactivation process in both HEK293 cells and cardiac myocytes in a voltage-dependent manner, indicating that NaV1.5 can give rise to persistent sodium current. Finally, by comparing both cell types under control settings, I found that transfected HEK293 cells inactivated at a much slower rate and at more negative potentials compared to the current in cardiac myocytes. My results suggest that NaV1.5 does not underlie oxidant-induced persistent current and that β subunits likely play a significant role in the inactivation process. / Thesis (Master, Physiology) -- Queen's University, 2011-08-19 14:46:42.665

No description available.

Thesis (Ph.D.) -- McMaster University, 1997. / Includes bibliographical references. Also available via World Wide Web.

Thesis (M.S.)--Virginia Polytechnic Institute and State University, 1992. / Vita. Abstract. Includes bibliographical references (leaves 123-127). Also available via the Internet.

Thesis (MS)--Montana State University--Bozeman, 2009. / Typescript. Chairperson, Graduate Committee: Brian Bothner. Includes bibliographical references (leaves 63-71).

Thesis (M.S.)--Marshall University, 2004. / Title from document title page. Document formatted into pages; contains x, 67 p. Includes abstract. Includes bibliographical references (p. 48-50).

Thesis (Ph. D.)--Columbia University, 1936. / Vita. Bibliography: p. 33.