Gordon L Kh, Valitova Iu N, Ogorodnikova T I, Rakhmatullina D F, Aliab'ev A Iu, Loseva N L, Tsentsevitskiĭ A N, Ruban N F
Tsitologiia. 2005;47(12):1088-94.
This paper reports changes in ion transport and energy metabolism of plant cells during short- and long-term expositions, resp., to antibiotic nystatin, which is known to specifically bind with plasma membrane sterols to form channels. The excised roots of 5 days old wheat seedlings were used as a model system in this research. It has been shown that treatment of excised roots with nystatin leads to activation of energy metabolism expressed as an increase of respiration and heat production by root cells. Furthermore, in the presence of nystatin increased pH of incubation medium, plasma membrane depolarization and a significant loss of potassium ions were observed. Nystatin-induced stimulation of respiration was prevented by malonate, an inhibitor of succinate dehydrogenase, electron acceptor dichlorophenolindophenol, and AgNO3, an inhibitor of H(+)-ATPase. Based on the data obtained it can be suggested that nystatin-induced stimulation of respiration is related to electron transport activation via mitochondrial respiratory chain, and is connected with activation of plasmalemma proton pump. Moreover, nystatin-induced increase of oxygen consumption was prevented by cerulenin, an inhibitor of fatty acid and sterol synthesis. This indicates that additional sterols and phospholipids may be synthesized in root cells to "heal" nystatin-caused damage of plasma membrane. A supposed chain of events of cell response to nystatin action may by as following: formation of nystatin channels-influx of protons--depolarization of plasmalemma-efflux of potassium ions-disturbance of ion homeostasis--activation of H(+)-ATPase work-increase in energy "requests" for H(+)-ATPase function--increase in the rate of oxygen consumption and heat production. The increased energy production under the action of nystatin, may provide the work of proton pump and synthesis of sterols and phospholipids, which are necessary for membrane regeneration.
本文报道了植物细胞在短期和长期分别暴露于抗生素制霉菌素期间离子转运和能量代谢的变化，已知制霉菌素能与质膜固醇特异性结合形成通道。本研究以5日龄小麦幼苗的离体根作为模型系统。结果表明，用制霉菌素处理离体根会导致能量代谢的激活，表现为根细胞呼吸作用和产热增加。此外，在制霉菌素存在的情况下，观察到孵育培养基的pH值升高、质膜去极化以及钾离子的大量流失。琥珀酸脱氢酶抑制剂丙二酸、电子受体二氯酚靛酚和H(+)-ATP酶抑制剂硝酸银可阻止制霉菌素诱导的呼吸刺激。根据所得数据可以推测，制霉菌素诱导的呼吸刺激与通过线粒体呼吸链的电子传递激活有关，并与质膜质子泵的激活有关。此外，脂肪酸和固醇合成抑制剂浅蓝菌素可阻止制霉菌素诱导的氧气消耗增加。这表明根细胞中可能会合成额外的固醇和磷脂来“修复”制霉菌素引起的质膜损伤。细胞对制霉菌素作用的反应可能的事件链如下：制霉菌素通道形成——质子内流——质膜去极化——钾离子外流——离子稳态紊乱——H(+)-ATP酶活性增加——对H(+)-ATP酶功能的能量“需求”增加——氧气消耗率和产热增加。制霉菌素作用下能量产生的增加可能为质子泵的工作以及膜再生所需的固醇和磷脂的合成提供能量。
