Katz A, Pick U
Department of Biological Chemistry, The Weizmann Institute of Science, 76100, Rehovot, Israel.
Biochim Biophys Acta. 2001 Apr 2;1504(2-3):423-31. doi: 10.1016/s0005-2728(01)00157-8.
The halotolerant alga Dunaliella adapts to exceptionally high salinity and maintains low Na(+) at hypersaline solutions, suggesting that it possesses efficient mechanisms for regulating intracellular Na(+). In this work we examined the possibility that Na(+) export in Dunaliella is linked to a plasma membrane electron transport (redox) system. Na(+) extrusion was induced in Dunaliella cells by elevation of intracellular Na(+) with Na(+)-specific ionophores. Elevation of intracellular Na(+) was found to enhance the reduction of an extracellular electron acceptor ferricyanide (FeCN). The quinone analogs NQNO and dicumarol inhibited FeCN reduction and led to accumulation of Na(+) by inhibition of Na(+) extrusion. These inhibitors also diminished the plasma membrane potential in Dunaliella. Anaerobic conditions elevated, whereas FeCN partially decreased intracellular Na(+) content. Cellular NAD(P)H level decreased upon enhancement of plasma membrane electron transport. These results are consistent with the operation of an electrogenic NAD(P)H-driven redox system coupled to Na(+) extrusion in Dunaliella plasma membrane. We propose that redox-driven Na(+) extrusion and recycling in Dunaliella evolved as means of adaptation to hypersaline environments.
嗜盐藻类杜氏盐藻能适应极高的盐度,并在高盐溶液中维持较低的胞内[Na⁺]浓度,这表明它拥有高效的细胞内Na⁺调节机制。在本研究中,我们探究了杜氏盐藻中Na⁺的排出是否与质膜电子传递(氧化还原)系统有关。通过使用Na⁺特异性离子载体提高细胞内Na⁺浓度,从而诱导杜氏盐藻细胞排出Na⁺。结果发现,细胞内Na⁺浓度升高会增强细胞外电子受体铁氰化物(FeCN)的还原。醌类似物NQNO和双香豆素抑制了FeCN的还原,并通过抑制Na⁺排出导致Na⁺积累。这些抑制剂还降低了杜氏盐藻的质膜电位。厌氧条件下细胞内Na⁺含量升高,而FeCN则使其部分降低。质膜电子传递增强时,细胞内NAD(P)H水平下降。这些结果与杜氏盐藻质膜中由电致NAD(P)H驱动的氧化还原系统与Na⁺排出相偶联的运作情况相符。我们认为,杜氏盐藻中由氧化还原驱动的Na⁺排出和循环是其适应高盐环境的一种方式。