XB-ART-18900Proc Natl Acad Sci U S A 1995 Dec 05;9225:11796-800.
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Susceptibility of cloned K+ channels to reactive oxygen species.
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.
PubMed ID: 8524851
PMC ID: PMC40489
Article link: Proc Natl Acad Sci U S A
Species referenced: Xenopus
Genes referenced: kcna2 kcna3 kcna4 kcna5 kcnb1 kcnb2 kcnc4 kcnd1 kcnj1 kcnj12 kcnj2 kcnj4 tert
References [+] :
Attali, Cloning, functional expression, and regulation of two K+ channels in human T lymphocytes. 1992, Pubmed, Xenbase