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首页> 外文期刊>American Journal of Physiology >Differential modulation of voltage-dependent K+ currents in colonic smooth muscle by oxidants.
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Differential modulation of voltage-dependent K+ currents in colonic smooth muscle by oxidants.

机译：氧化剂对结肠平滑肌中电压依赖性K +电流的差分调节。

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The effect of oxidants on voltage-dependent K+ currents was examined in mouse colonic smooth muscle cells. Exposure to either chloramine-T (Ch-T), an agent known to oxidize both cysteine and methionine residues, or the colon-specific oxidant monochloramine (NH2Cl) completely suppressed the transient outward K+ current (Ito) while simultaneously enhancing the sustained delayed rectifier K+ current (Idr). In contrast, the cysteine-specific oxidants hydrogen peroxide (H2O2) and 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB) exhibited partial and slow suppression of Ito by inducing a shift in channel availability of -18 mV without affecting Idr. After enhancement by NH2Cl or Ch-T, Idr was sensitive to 10 mM tetraethylammonium but not to other K+ channel blockers, suggesting that it represented activation of the resting Idr and not a separate K+ conductance. Extracellular dithiothreitol (DTT) partially reversed the effect of H2O2 and DTNB on Ito but not the actions of NH2Cl and Ch-T on either Idr or Ito. Dialysis of myocytes with GSH (5 mM) or DTT (5 mM) prevented suppression of Ito by H2O2 and DTNB but did not alter the effects of NH2Cl or Ch-T on either Idr or Ito. Ch-T and NH2Cl completely blocked Ito generated by murine K(v)4.1, 4.2, and 4.3 in Xenopus oocytes, an effect not reversible by intracellular DTT. In contrast, intracellular DTT reversed the effect of H2O2 and DTNB on the cloned channels. These results suggest that I(to) is suppressed via modification of both methionine and cysteine residues, whereas enhancement of Idr likely results from methionine oxidation alone.
机译：在小鼠结肠平滑肌细胞中检查了氧化剂对电压依赖性K +电流的影响。暴露于氯胺-T（Ch-T）（一种已知能同时氧化半胱氨酸和蛋氨酸残基的试剂）或结肠特异性氧化剂一氯胺（NH2Cl），可以完全抑制瞬时向外K +电流（Ito），同时增强持续的延迟整流器K +电流（Idr）。相反，半胱氨酸特异性氧化剂过氧化氢（H2O2）和5,5'-二硫代双（2-硝基苯甲酸）（DTNB）通过诱导-18 mV的通道可用度变化而对Ito表现出部分和缓慢的抑制作用，而不会影响Idr 。在被NH2Cl或Ch-T增强后，Idr对10 mM四乙基铵敏感，但对其他K +通道阻滞剂不敏感，表明它代表静止的Idr的活化，而不是单独的K +电导。细胞外二硫苏糖醇（DTT）可以部分逆转H2O2和DTNB对Ito的作用，但不能逆转NH2Cl和Ch-T对Idr或Ito的作用。用GSH（5 mM）或DTT（5 mM）透析心肌细胞可防止H2O2和DTNB对Ito的抑制，但不会改变NH2Cl或Ch-T对Idr或Ito的影响。 Ch-T和NH2Cl完全阻断了非洲爪蟾卵母细胞K（v）4.1、4.2和4.3产生的Ito，这种作用是细胞内DTT无法逆转的。相反，细胞内DTT逆转了H2O2和DTNB对克隆通道的作用。这些结果表明，I（to）通过蛋氨酸和半胱氨酸残基的修饰而被抑制，而Idr的增强很可能仅由蛋氨酸氧化引起。

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