Modifications of Human Cardiac Sodium Channel Gating by UVA Light

Modifications of Human Cardiac Sodium Channel Gating by UVA Light Voltage-gated Na+ channels are membrane proteins responsible for the generation of action potentials. In this report we demonstrate that UVA light elicits gating changes of human cardiac Na+ channels. First, UVA irradiation hampers the fast inactivation of cardiac Nav1.5 Na+ channels expressed in HEK293t cells. A maintained current becomes conspicuous during depolarization and reaches its maximal quasi steady-state level within 5–7 min. Second, the activation time course is slowed by UVA light; modification of the activation gating by UVA irradiation continues for 20 min without reaching steady state. Third, along with the slowed activation time course, the peak current is reduced progressively. Most Na+ currents are eliminated during 20 min of UVA irradiation. Fourth, UVA light increases the holding current nonlinearly; this phenomenon is slow at first but abruptly fast after 20 min. Other skeletal muscle Nav1.4 isoforms and native neuronal Na+ channels in rat GH3 cells are likewise sensitive to UVA irradiation. Interestingly, a reactive oxygen metabolite (hydrogen peroxide at 1.5%) and an oxidant (chloramine-T at 0.5 mM) affect Na+ channel gating similarly, but not identically, to UVA. These results together suggest that UVA modification of Na+ channel gating is likely mediated via multiple reactive oxygen metabolites. The potential link between oxidative stress and the impaired Na+ channel gating may provide valuable clues for ischemia/reperfusion injury in heart and in CNS. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Modifications of Human Cardiac Sodium Channel Gating by UVA Light

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Publisher
Springer-Verlag
Copyright
Copyright © 2002 by Springer-Verlag New York Inc.
Subject
Life Sciences; Biochemistry, general; Human Physiology
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s00232-002-1010-z
Publisher site
See Article on Publisher Site

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