All ETDs from UAB

Advisory Committee Chair

Sadis Matalon

Advisory Committee Members

Michelle V Fanucchi

Rakesh P Patel

Edward M Postlethwait

Document Type

Thesis

Date of Award

2010

Degree Name by School

Master of Science in Public Health (MSPH) School of Public Health

Abstract

Rationale: Nitrite (NO2-) has been shown to limit injury to the heart, liver and kidneys in various models of ischemia-reperfusion injury. Currently, potential protective effects of systemic NO2- in limiting lung injury or enhancing repair have not been documented. Objectives: To assess the efficacy and mechanisms by which post-exposure intra-peritoneal injections of NO2- mitigate Cl2 induced lung injury in rats. Methods: Rats were exposed to Cl2 (400 ppm) for 30 minutes and returned to room air. Nitrite (1mg/Kg) or saline were administered intraperitoneally at 10 min, 2, 4 and 6 hrs post exposure. Rats were sacrificed at 6 hrs or 24 hrs and injury to airway and alveolar epithelia was assessed by morphology, protein concentrations, number of cells in bronchoalveolar lavage (BAL) and wet/dry lung weights. Lipid peroxidation was assessed by measuring lung F2-isoprostanes. Results: Rats developed severe but transient hypoxemia. At 6 hrs post-Cl2 exposure, protein concentration, the number of neutrophils, and lung wet/dry weights increased significantly. Quantitative morphology revealed extensive lung injury in the upper airways; airway epithelial cells stained positive for TUNEL, but not caspase-3. Administration of NO2- resulted in lower BAL protein levels, significant reduction in the intensity of the TUNEL positive cells and normal values of lung wet/dry weights. F2-isoprostane levels increased at six and 24 h post Cl2 exposure in both NO2- and saline injected rats. Conclusion: This is the first time demonstration that systemic nitrite administration mitigates airway and epithelial injury. Key words: pulmonary edema, apoptosis, necrosis, isoprostanes, airway injury

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