摘要:
研究了NADPH氧化酶在ABA(abscisicacid)诱导蚕豆气孔关闭信号转导网络中的作用,荧光光谱实验表明,在嗜中性白血球NADPH氧化酶抑制剂DPI(diphenyleneio-donium)存在的条件下,与对照相比,大大逆转了由ABA引起HPTS(8-hydroxypyrene-1,3,6-trisulfonicacid,trisodiumsalt)的荧光强度下降。表皮生物分析法显示,10-6mol/L的DPI和103unit/mL的过氧化氢酶(catalase,CAT)在一定程度上也逆转了ABA诱导张开气孔的关闭。因此推测:在ABA诱导蚕豆气孔保卫细胞过程中,质膜上的NADPH氧化酶可能催化形成超氧自由基O2,再经歧化反应形成H2O2,而形成的H2O2参与了气孔运动调节。
Abstract:
The mechanisms of H2O2 generation in guard cells of Vicia faba induced by abscisic acid (ABA) were measured by using fluorescene probe, 8-hydroxypyrene-1,3,6-trisulfonic acid, trisodium salt (HPTS). When guard cells were treated with ABA, fluorescene quenching of HPTS occurred, and the treatment of the guard cells with diphenyleneiodonium(DPI) at 10-6 mol/mL (final concentration) which is known as an inhibitor of supero xide generating NADPH oxidases nearly reversed the quenching reaction induced by ABA O2 mmol/L(final concentration). ABA and H2O2 might induce stomatal closure. Furthermore, when DPI or catalase(CAT)(103 unit/mL) was added to the suspension after above treatment reversed ABA-induced stomatal closure. These results suggest that a novel O2 generating NADPH oxidase in the plasma membrane of guard cell of Vicia faba may be activated by ABA, and subsequently H2O2, which involved in the signal transduction pathway of ABA-induced stomatal closure.