PubMed 8524851

Referenced in: none

Automatically associated channels: Kir1.1 , Kir2.1 , Kir2.3 , Kv1.2 , Kv1.3 , Kv1.4 , Kv1.5 , Kv2.1 , Kv2.2 , Kv3.1 , Kv3.4 , Kv4.1

Title: Susceptibility of cloned K+ channels to reactive oxygen species.

Authors: F Duprat, E Guillemare, G Romey, M Fink, F Lesage, M Lazdunski, E Honore

Journal, date & volume: Proc. Natl. Acad. Sci. U.S.A., 1995 Dec 5 , 92, 11796-800

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/8524851

Abstract
Free radical-induced oxidant stress has been implicated in a number of physiological and pathophysiological states including ischemia and reperfusion-induced dysrhythmia in the heart, apoptosis of T lymphocytes, phagocytosis, and neurodegeneration. We have studied the effects of oxidant stress on the native K+ channel from T lymphocytes and on K+ channels cloned from cardiac, brain, and T-lymphocyte cells and expressed in Xenopus oocytes. The activity of three Shaker K+ channels (Kv1.3, Kv1.4, and Kv1.5), one Shaw channel (Kv3.4), and one inward rectifier K+ channel (IRK3) was drastically inhibited by photoactivation of rose bengal, a classical generator of reactive oxygen species. Other channel types (such as Shaker K+ channel Kv1.2, Shab channels Kv2.1 and Kv2.2, Shal channel Kv4.1, inward rectifiers IRK1 and ROMK1, and hIsK) were completely resistant to this treatment. On the other hand tert-butyl hydroperoxide, another generator of reactive oxygen species, removed the fast inactivation processes of Kv1.4 and Kv3.4 but did not alter other channels. Xanthine/xanthine oxidase system had no effect on all channels studied. Thus, we show that different types of K+ channels are differently modified by reactive oxygen species, an observation that might be of importance in disease states.