Journal of Applied Physiology AJP: Endocrinology and Metabolism
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J Appl Physiol (September 26, 2003). doi:10.1152/japplphysiol.00002.2003
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Submitted on January 3, 2003
Accepted on July 30, 2003

Hypochlorous acid alters bronchial epithelial cell membrane properties and prevention by extracellular glutathione

Charles J Venglarik1, Julio Giron-Calle2, Amanda F Wigley1, Ernst Malle3, Nobuo Watanabe1, and Henry Jay Forman4*

1 Department of Environmental Health Sciences, University of Alabama at Birmingham, School of Public Health, Birmingham, AL, USA
2 Department of Environmental Health Sciences, University of Alabama at Birmingham, School of Public Health, Birmingham, AL, USA; Departamento de Fisiologia y Tecnolgia de Productos Vegetales, Instituto de la Grasa, Sevilla, Spain
3 Institute of Medial Biochemistry and Medical Molecular Biology, Karl-Franzens University, Graz, Austria
4 Department of Environmental Health Sciences, University of Alabama at Birmingham, School of Public Health, Birmingham, AL, USA; Division of Natural Sciences, University of California Merced, Merced, CA, USA

* To whom correspondence should be addressed. E-mail: hforman{at}ucmerced.edu.

In chronic inflammatory diseases of the airways, such as cystic fibrosis, hypochlorous acid (HOCl) generated by neutrophils is involved in airway injury. We examined the effects of HOCl on 16HBE14o- bronchial epithelial cells by bolus addition or by generation with glucose oxidase plus myeloperoxidase. HOCl produced both carbonyl formation of a discreet number of proteins and modification of surface targets that were recognized by an antibody raised against HOCl-modified protein. Bolus or enzymatically generated HOCl decreased transepithelial resistance but surprisingly, bolus HOCl also increased short-circuit current. Glutathione in lung epithelial lining fluid (ELF) is an excellent scavenger of HOCl; however, glutathione content is lower in cystic fibrosis ELF due to deficient glutathione transport to the apical side of bronchial-tracheal epithelial cells (Gao et al., Am. J. Physiol. 277:L113-8, 1999). We found that alteration of the GSH content of apical fluid above 16HBE14o- cells was protective as all HOCl induced changes were delayed or eliminated by exogenous glutathione within the physiological range. Extrapolating this to cystic fibrosis, suggests that HOCl can alter cell function without destruction but that elevating glutathione could be protective.




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