Warenycia M W, Steele J A, Karpinski E, Reiffenstein R J
Department of Pharmacology, University of Alberta, Edmonton, Canada.
Neurotoxicology. 1989 Summer;10(2):191-9.
Patch clamp studies of neuroblastoma cells have shown that in the presence of sodium hydrogen sulfide (NaHS; the in vitro precursor of H2S), addition of the sulfonated amino acids, taurine or cysteic acid resulted in reversible abolition of the inward sodium currents. This effect could also be demonstrated by preincubating cells for 3-20 min with 5-10 mM NaHS followed by replacement of the solution with taurine or cysteic acid in sulfide-free saline. Neither NaHS, taurine nor cysteic acid alone had any effect. The sulfhydryl reagents, beta-mercaptoethanol and dithiothreitol, were also found to abolish reversibly the sodium currents. As the effects of the above treatments were nearly identical, the synergistic action of NaHS with taurine or cysteic acid may result from reduction of the disulfide bonds between subunits comprising the sodium channel. The responses to NaHS and taurine, a putative neurotransmitter/neuromodulator, suggest that reductions in sodium channel function may be the mechanism(s) responsible for loss of central respiratory drive during H2S poisoning.
神经母细胞瘤细胞的膜片钳研究表明，在存在硫化氢钠（NaHS；H2S的体外前体）的情况下，添加磺化氨基酸、牛磺酸或半胱磺酸会导致内向钠电流可逆性消失。通过用5-10 mM NaHS将细胞预孵育3-20分钟，然后用无硫化物盐水中的牛磺酸或半胱磺酸替换溶液，也可以证明这种效应。单独的NaHS、牛磺酸或半胱磺酸均无任何作用。巯基试剂β-巯基乙醇和二硫苏糖醇也被发现可可逆地消除钠电流。由于上述处理的效果几乎相同，NaHS与牛磺酸或半胱磺酸的协同作用可能是由于构成钠通道的亚基之间的二硫键减少所致。对NaHS和牛磺酸（一种假定的神经递质/神经调节剂）的反应表明，钠通道功能的降低可能是H2S中毒期间中枢呼吸驱动丧失的机制。
