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Mechanisms Of Hyperglycemia-Induced Ros Production In Osmotically Swollen Glial Cells, Augusta K. Eduafo
Mechanisms Of Hyperglycemia-Induced Ros Production In Osmotically Swollen Glial Cells, Augusta K. Eduafo
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Cerebral edema is a potentially fatal complication of diabetes. There is evidence for increased Reactive Oxidative Species (ROS) production during cerebral edema in diabetics. This can lead to oxidative stress, thought to contribute to the onset and progression of diabetes and can cause cell injury and cell death. ROS, in moderate amounts, are involved in physiological processes within the body that produce favorable cellular responses. Unfortunately, high levels of ROS can lead to cellular damage of lipids, membranes, proteins and DNA. Hyperglycemia can cause an increase in ROS production due to activation of NADPH oxidases. The purpose of this study …
Oxidative Stress And Cell Death In Osmotically Swollen Glial Cells, Crystal Elaine Stuckey
Oxidative Stress And Cell Death In Osmotically Swollen Glial Cells, Crystal Elaine Stuckey
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Regulation of normal volume is an important aspect of cell homeostasis. Possible mechanisms which signal volume regulation are increasing the rate of reactive oxygen species (ROS) production and release of ATP for interaction with purinergic receptors. We examined whether an increase in ROS production during cell swelling also led to cell injury of C6 glioma cells. Cells were loaded with 5,6-carboxy-2,7-dihydrofluorscein diacetate (DCFDA) to fluoroscopically measure the rate of cellular ROS production and were perfused with phosphate-buffered saline solutions (PBS) containing 100 μM carbenoxolone to inhibit dye efflux. Cell death was determined cytometrically and by measuring the release of lactate …
The Relationship Between Lactic Acid, Reactive Oxygen Species And The Hypoxia-Induced Acidification Seen In Chemosensitive Neurons Of The Nucleus Tractus Solitarius (Nts), Trevor Downing
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The NTS is one of many sites of chemoreception meaning that it responds to changes in CO2 and pH. NTS neurons also acidify approximately 0.13 pH units in response to hypoxia. Experiments involved brainstem slices exposed to a control hypoxic bout followed by hypoxia in conjunction with different drugs. The drugs included fluorocitrate, 4-hydroxycinnamate, oxygen-glucose deprivation and iodoacetate. Iodoacetate produced the strongest blunting of the hypoxia-induced acidification and decreased the response by ~53%. Results from the studies using the superoxide probe DHE showed an increase in the levels of ROS during the hypoxic exposure prior to reoxygenation. Two ROS scavengers …