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Oxidant-mediated ciliary dysfunction in human respiratory epithelium


, : Oxidant-mediated ciliary dysfunction in human respiratory epithelium. Free Radical Biology & Medicine. 17(1): 1-10

Exposure of human nasal ciliated epithelium to reactive oxidants generated by the enzymatic xanthine-xanthine oxidase superoxide/hydrogen peroxide (H-2O-2) and glucose-glucose oxidase H-2O-2-generating systems, or to reagent H-2O-2 or hypochlorous acid (HOCl) resulted in significant alterations in ciliary beating. The earliest change noted was the presence of ciliary slowing, progressing eventually to complete ciliary stasis in some areas. Ciliary dyskinesia was seen within the first hour, often from as early as 15 min after exposure of the cells to reactive oxidants. Using peroxidases, various antioxidant enzymes, and oxidant scavengers, we confirmed that these detrimental effects on ciliary function were mediated primarily by H-2O-2 and HOCl. Moreover, 3-aminobenzamide (3-ABA), an inhibitor of the DNA repair enzyme poly ADP ribose polymerase, prevented H-2O-2-mediated inhibition of ciliary function, indicating that oxidant-mediated damage to DNA may well be the basis of the effects of H-2O-2 on ciliated epithelium. Acute and chronic inflammatory responses may therefore present the possible threat of H-2O-2- or HOCl-inflicted injury on bystander respiratory epithelium, leading to ciliary dyskinesia and slowing.

US$19.90

PMID: 7959161

DOI: 10.1016/0891-5849(94)90002-7


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