Effecte of hyperoxia in bovine bronchail epithelial tissue Dissertation

Effecte of hyperoxia in bovine bronchail epithelial tissue - Dissertation Example Important Use of Hyperoxia in Intensive Care Unit Hyperoxic inspired gas is essential for patients with hypoxic respiratory failure which can be caused by oxygen deficient conditions like acute infection, neuromuscular impairment, etc. (Altemeler and Sinclair, 2007) In the context of critical care medicine, hyperoxia can be beneficial in implementing certain critical care strategies like early goal directed therapy (Calzia et al, 2010). Moreover, oxygen pressure field theory suggests that hyperoxia just before deep hypoxic circulatory arrest takes advantage of increased oxygen solubility and reduced oxygen consumption to load tissues with excess oxygen, which can effectively manage acid-base states during acute hypothermia entailed in circulatory arrest (Pearl et al, 2000) However, studies also testify that hyperoxia adversely affects cilial abundance and cause ciliary disorientation which can lead to dangerous conditions like ciliary dyskinesia (MacNaughton et al, 2007; Kay et al, 2 002; Rutman et al, 1993). Also, hyperoxia may impede the pathways of cell signalling (Lee and Choi, 2003) Side Effects of Reactive Oxygen Species (ROS) on Epithelial Tissue Reactive Oxygen Species (ROS) are oxygen containing molecules which are highly reactive. The unpaired valance shell electrons in ROS are responsible for their high reactivity. ROS are often regarded as a key factor behind cardiovascular diseases, ischemic injury, programmed cell death, etc. They can also cause damage to DNA, lipid peroxidation and critical oxidative stress. (Thannickal, 2003; Fuhrman et al 1997) ROS would cause oxidative stress on the epithelial tissue by increasing the levels of total glutathione. Since glutathione is an anti-oxidant, increased levels of ROS will increase its concentration as well. In the case of glutathione depletion, increase of ROS levels is unbridled which would lead to early activation of apoptic signalling. In vivo studies involving human B lymphoma cell line testify such possibilities (Armstrong et al, 2002). Moreover, it has also been testified that pulmonary macrophages stimulate cell proliferation of bovine bronchial epithelial cells in vitro. The process involves mediation in airway epithelial repair, which can probably be explained by a proactive role of glutathione against ROS (Takizawa et al, 1990). Another side effect of ROS is lipid peroxidation which has been studied in details through epithelial cell behaviour in vivo in rats with chronic parenchymal iron overload (Bacon et al, 1983). Hepatic and brain epithelial lipid peroxidation by ROS obtained from certain pesticides have been widely testified by both in vivo and in vitro studies in rats and humans (Bagchi et al, 1995). Besides, Fuhrman and his associates conducted in vitro and ex vivo studies in humans to testify the high extent of low-density-lipoprotein oxidation by ROS through measurement of thiobarbituric acid reactive substances (TBARS) and lipid peroxides in epithelial cells (F uhrman et al, 1997). Proteins modification is another major side effect of excess ROS generation that has been studied in vivo. The in vivo study conducted in this context further testified that oxidative protein damage could affect the activities of the DNA repair enzymes in the epithelial cells as well (Wiseman and Halliwell, 1996). Further, in vitro studies have established that generation of ROS target the function of redox-sensitive proteins that act as part of a large sub-membranous