mixture up to 52 times when compared with oil alone. Several in-vivo studies using murine models of exposure have demonstrated alterations caused in the cardiovascular, neurologic, and PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19762596 immune systems by CE. Despite the large volume of CE used in remediation, the effects on the respiratory epithelium of humans and gills of aquatic animals such as fish and crabs exposed to this dispersant are largely unknown. The respiratory epithelium is a monolayer of cells that provides a continuous, critical, and a highly regulated barrier to environmental insults in human airways and in the gills of aquatic animals. The zebrafish has become a premier fish model for studies related to aquatic toxicology as well as human health. More specifically, the gill has been identified as an important tissue of interest in assessing toxic exposure. Inflammation of these mucosal respiratory membranes can lead to a loss of integrity of the epithelium, edema, increase in the permeability of the epithelial monolayer, and a diminished capacity to limit submucosal access by environmental toxins leading to an increased risk of developing complications. Furthermore, sustained damage to this tissue may also initiate an edematous and inflammatory response in the epithelium leading to obstruction of the airways in humans with exacerbation of pre-existing respiratory diseases such as asthma. Using human BEAS-2B epithelial cells, Shi et al found that CE could induce reactive oxygen species generation and autophagy but without marked apoptosis. However, another study in BL16/BL6 cells indicated that CE could alter the intracellular oxidative states and lead to mitochondrial dysfunction and apoptosis, suggesting the important role of oxidative balance in CE-induced cell injury. Many studies have reported that ROS play an important role in inducing DNA damage, mitochondrial dysfunction and apoptosis. Heme oxygenase1 is a cytoprotective enzyme in epithelial and other cell types. HO-1 is involved in the degradation of heme with generation of effective anti-inflammatory molecules such as carbon monoxide, iron, and biliverdin, which possess potent anti-apoptotic properties. Induction of HO-1 and CO results in protection against various PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19761586 oxidant-mediated inflammatory responses in lung, liver and cartilage. In contrast, zinc protoporphyrin, which acts as an HO-1 activity inhibitor, enhances lipid peroxidation and decreases glutathione content by reversing the effects of hemin, an HO-1 inducer. HO-1 also protects endothelial cells and renal epithelial cells against 2883-98-9 price apoptosis induced by oxidative stress. The inhibition of ROS and apoptosis appears to be one of the major mechanisms underlying the cytoprotective function of HO-1. However, there is limited investigation in the role of HO-1 in CE-induced production of ROS and apoptosis. ROS are produced by a series of enzymes such as cytochrome 450, lipooxygenase, and NADPH oxidase complex, as well as an acute phase reactant C-reactive protein . Activation of NOX4 in melanoma cells, myocardial cells, mesangial cells, and airway epithelial cells mediates oxidative stress-induced apoptosis. Extracellular generation of H2O2 via NOX4 induction by lung epithelial cells may mediate additional effects in tissues via induction of cell apoptosis by a paracrine mechanism or by inducing 2 / 23 HO-1 Protects against Corexit-Induced Apoptosis matrix-crosslinking reactions in the presence of extracellular heme peroxidases. CRP directly induces NOX activa

Fluorescence images of were analyzed to calculate the nuclear-to-total fluorescence ratio

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