Effects of hypochlorite on cultured respiratory epithelial cells

Neutrophils pathogenesis of many respiratory diseases. The enzymes myeloper oxidase and eosinophil peroxidase catalyze the reaction of H2O2 with Cl to produce the reactive oxygen species HOCl. Normal human bronchial epithelial (NHBE) cells were exposed to 0.18-0.90 mM HOCl for 48 h, and studied with immunohistochemical, metabolic and morphol ogical studies. The ability of the cells to attach to each other and/or to the matrix was altered. Immunohistochemical studies showed a decreased amou nt of desmosomes and focal adhesion sites, although the morphology of the c ells was not affected. The ability of the mitochondria to oxidize glucose was reduced. HOCl-expose d cells had an increased production of NO, Probably by an increased activit y of cNOS, due to increased intracellular Ca2+. The antioxidant N-acetyl-cy steine inhibited both the NO production and the effects of HOCl on glucose oxidation. The cNOS-inhibitor N-propyl-L-arginine inhibited HOCl-induced NO production. X-ra) microanalysis showed an increase in the intracellular Na +/K+ ratio, which indicates cell damage. In conclusion exposure to HOCl results in cell detachment and metabolic alt erations in normal human bronchial epithelial cells. Oxygen radicals could in part mediate the effects. Oxygen radicals could hence contribute to the observed epithelial damage in respiratory diseases.