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This dissertation, Impact of Gestational Diabetes Mellitus on Placental Thioredoxin System by Chi-wai, Lee, 李志慧, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: ABSTRACT of thesis entitled Impact of Gestational Diabetes Mellitus on Placental Thioredoxin System Submitted by LEE CHI WAI for the degree of Master of Philosophy at The University of Hong Kong in August 2007 Gestational diabetes mellitus (GDM) is defined as glucose intolerance with its first onset recognized during pregnancy. The hyperglycemia and metabolic disturbance in GDM can induce oxidative stress and reduce the activity of the placental antioxidant enzymes. The increase in oxidative stress in these patients contributes to the increase in tissues damage and is associated with adverse perinatal outcome. Thioredoxin (Trx) is a small multifunctional protein ubiquitously expressed in many different tissues. It has two main isoforms termed Trx1 and Trx2, and are localized in the cytosol and mitochondria respectively. These two proteins are important thiol- containing antioxidants in cells and can function as anti-apoptotic proteins. Expressions of the two Trxs are found in normal human placenta, with Trx1 being localized in the trophoblastic region and plays a protective role against oxidative stress. Here, a prospective study was carried out in which high-risk women were 1recruited from the clinic for placental studies on oxidative stress and cell death. Following delivery, placental specimens were collected and placental protein carbonyl content was measured by western blot analysis to examine the oxidative stress status. It was found to be significantly increased in diabetic pregnancies in comparison to pregnancies with normal glucose tolerance (NGT). In addition, a significant increase in Trx1 protein was demonstrated in the GDM group, while this change was not observed in Trx2. With immunohistochemistry technique, the enhanced expression of placental Trx1 was mainly localized in the trophoblastic region of the placental villi, and this may indicate a role in the protection against oxidative stress in responses to maternal GDM. In order to study the molecular control for placental Trx1 and Trx2, their mRNA expressions were also examined. However, no significant difference was formed between GDM and NGT pregnancies. To examine the relationship between oxidative stress and apoptosis in the placenta and the relationship with the Trx system, ASK-1 expression and caspase 3 activation were measured and correlated with the protein carbonyl contents and Trx1. Significant positive correlation was observed between the expression of Trx1 and ASK-1; while significant negative correlation was observed between protein carbonyl contents and caspase 3 activation. Taking together, we have demonstrated increased protein carbonyl contents and enhancement of Trx1 content in placentas from GDM pregnancies. Further investigations are warranted to elucidate the functional role of the Trx system in the protection against oxidative stress and the placentas of pregnancies complicated by GDM. 2 DOI: 10.5353/th_b3955889 Subjects: Diabetes in pregnancyThioredoxin

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