S [1]. A common causative factor of ALI is lipopolysaccharide (LPS), an
S [1]. A common causative factor of ALI is lipopolysaccharide (LPS), an endotoxin present in the bacterial outer membrane [2]. Typical manifestations of ALI are alveolar and airway inflammatory response [3,4], the presence of inflammatory cells and proteinaceous fluid in air spaces [5,6], increased microvascular permeability due to endothelial barrier disruption [7,8], bronchoalveolar cell death [9],* Correspondence: [email protected] Contributed equally Department of Pharmaceutical Sciences, St. John’s University, College of Pharmacy and Allied Health Professions, 8000 Utopia Parkway, Jamaica, New York 11439, USA Full list of author information is available at the end of the articleand cellular changes suggestive of lung inflammation and/or injury [10]. One major contributory factor to the pathogenesis of ALI is the release of reactive oxygen species (ROS) and reactive nitrogen species (RNS), proteolytic enzymes, lipid mediators and proinflammatory cytokines principally from neutrophils and alveolar and interstitial macrophages [9]. The ensuing overwhelming oxidative and nitrosative stresses [10,11], in turn, cause direct damage PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28549975 to DNA [9], apoptosis [12], deplete reduced glutathione (GSH) stores [13-15], promote lipid peroxidation (LPO)[16,17], protein nitration and protein activity alteration [18,19], inactivate antioxidant and antiproteinase enzymes [9], and activate transcriptional factors mediating the expression of proinflammatory genes in phagocytic cells and in endothelial and epithelial lung cells [9,20-22].?2010 Lau-Cam et al; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Bhavsar et al. Journal of Biomedical Science 2010, 17(Suppl 1):S19 http://www.jbiomedsci.com/content/17/S1/SPage 2 ofThe relevance of oxidative stress to the development of ALI is supported by the results of studies in experimental animal models of ALI demonstrating that low molecular weight antioxidant compounds possessing a wide range of structural features and biological activities are able to decrease the severity of the inflammatory process by reducing the migration of macrophages, monocytes and neutrophils into the lung [23] and the production of ROS and RNS by these cells [24,25]. One of the compounds that has demonstrated protective actions in the lung against inflammation by LPS and other exogenous agents is taurine (TAU), a nonprotein amino acid with a ubiquitous distribution and a high concentration in human tissues. As an antioxidant, TAU is rather unique since it is able to attenuate LPO and the loss of intracellular antioxidant defenses under conditions of oxidative stress in spite of lacking a readily oxidizable functionality [26] and has the ability to selectively AUY922 biological activity scavenge free radicals generated during ALI [27,28]. For example, the addition of this compound to cultured pneumocytes was found to reduce the LPSinduced generation of ROS and the activation of mitogen-activated protein kinases and Bax [29]; and the pretreatment of rats with 5 TAU in the drinking water resulted in a lower number of inflammatory leukocytes infiltrating the lung and in attenuation of the focal bronchiolar hyperplasia that developed from a short contact with ozone [30]. Moreover, an earlier study from this laboratory.
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