Autor: |
Jeulin, C., Fournier, J., Marano, F., Dazy, A.-C. |
Předmět: |
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Zdroj: |
Pflügers Archiv: European Journal of Physiology; Jan2000, Vol. 439 Issue 3, p331-338, 8p |
Abstrakt: |
Respiratory pathologies can result from the exposure of airway epithelial cells to oxidative stress. We studied the effects of the hydroxyl radical ⨰OH, for which there is no natural intra- or extracellular scavenger, on an outwardly rectifying chloride channel (ORCC). In the human bronchial cell line 16HBE14o–, the cytoplasmic side of ORCC in inside-out excised membrane patches was exposed to ⨰OH created by simultaneously superfusing Fe2+ and H2O2 in front of the patch-pipette. ORCC was activated by depolarizing voltage steps. Its open probability (Po) increased with bath [Ca2+] above 1 µM. Upon brief exposure to ⨰OH, ORCC first closed and then alternated between periods of closure and normal activity. The duration of closure increased with the duration of ⨰OH exposure but voltage steps could reopen the channel. After 10 min exposure to ⨰OH, however, the channel closed irreversibly, regardless of the number of subsequent voltage steps or the duration of washing. Low [Ca2+] in the bath accelerated the irreversible closure of the channel in the presence of ⨰OH. Intracellular application of ⨰OH progressively inhibited ORCC activity by inducing long closure periods that increased with time. This might have important pathophysiological implications in the process of inflammation. [ABSTRACT FROM AUTHOR] |
Databáze: |
Complementary Index |
Externí odkaz: |
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