Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04179 (MnSOD)
 2,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cells living under aerobic conditions always face an oxygen paradox. Oxygen is necessary for cells to maintain their lives. However, toxic reactive oxygen species such as the superoxide radical, the hydroxyl radical and hydrogen peroxide are generated from oxygen and damage cells. Oxidative stress occurs as a consequence of excessive production of reactive oxygen species or impaired antioxidant defense systems. Antioxidant enzymes include two types of superoxide dismutase (SOD), which specifically scavenges superoxide radicals: copper-zinc SOD, which is located in the cytosol and Mn-SOD, which is located in the mitochondria. SOD is the first enzymatic step in the defense system against oxidative stress. In addition to ovarian steroid hormones, a number of local factors such as cytokines, growth factors and eicosanoids have been reported to be involved in the regulation of endometrial function. Recently, much attention has been focused on the finding that reactive oxygen species act as second messengers in the regulation of cellular function. Since reactive oxygen species are generated, and SOD is expressed, in the endometrium, it is possible that reactive oxygen species and SOD work as local regulators of endometrial function. The present review summarizes recent findings that reactive oxygen species and SOD play important roles in the process of reproductive physiology such as decidualization and menstruation in the human endometrium.
Placenta 2007 Apr
PMID:The role of oxygen radical-mediated signaling pathways in endometrial function. 1729 83

Maternal diabetes affects the development of the offspring by altering the uterine environment. We aimed to investigate the extent to which the blood flow (measured as Tissue Perfusion Units; TPU) to implantation sites and the expression of developmentally important genes in the offspring are affected by maternal diabetes. We measured mRNA levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), Bcl-2 associated X protein (Bax), B-cell lymphoma protein (Bcl-2), tumor suppressor protein-53 (p53), paired box protein-3 (Pax-3) and vascular endothelial growth factor-A (Vegf-A). Moreover, we studied the effect on uterine blood flow (TPU) and the expression of the genes exerted by embryonic maldevelopment (malformation or resorption). Streptozotocin induced diabetic (D) and non-diabetic (N) pregnant rats were used in the study. Blood flow (TPU) to implantation sites was measured by a laser Doppler flow meter, and gene expression was analyzed by RT-PCR. Maternal diabetes caused increased blood flow (TPU) to implantation sites compared with normal pregnancy. Furthermore, implantation sites of D rats containing malformed offspring showed impaired growth and decreased blood flow (TPU) compared with their littermates at all gestational days. Resorbed offspring from both N and D rats displayed increased blood flow (TPU) compared with their non-resorbed littermates. Moreover, we found that maternal diabetes causes decreased expression of genes involved in the oxidative stress defense system (CuZnSOD in non-malformed D11 embryos, MnSOD at all gestational time points, ECSOD and Gpx-1 at GD11-GD15, CAT and Gpx-2 at GD15), decreased expression of Pax-3 at GD11, and increased expression of Vegf-A at all gestational time points. We conclude that both maternal metabolism and embryonic developmental state affect the blood flow (TPU) to the implantation site. Maternal diabetes causes decreased expression of anti-oxidative enzymes and enhanced angiogenesis in the offspring in rats.
Placenta 2008 May
PMID:Altered uterine perfusion is involved in fetal outcome of diabetic rats. 1838 70