The unicellular halotolerant alga Dunaliella salina had the ability to oxidize NADH and reduce Fe(CN)63-.The redox reactions were to some extent stimulated by slight hyperosmotic shock (2.0mol/L→2.6mol/L NaCl),but markably inhibited by abrupt hyperosmotic shock (2.0mol/L→3.5mol/L NaCl) and hypoosmotic shock (2.0mol/L→1.0mol/L NaCl;2.0mol/L→0.67mol/L NaCl).With the adaptation of algal cells to osmotic shock by accumulating or degraging intracellular grycerol,the plasmalemma redox activities were also restored.The O2 uptake stimulated by NADH could be promoted by FA and SHAM.Hypoosmotic shock increases the basal respiration rate of alga cells,but weakened the stimulating effects of NADH,FA and SHAM on O2 uptake.On the other hand,hyperosmotic shock reduced the basal respiration rate,but relatively enhanced the above effects of NADH,FA and SHAM.H+ extrusion of alga cells was inhibited by NADH and stimulated by Fe(CN)63-.Vanadate and DES could inhibit H+ efflux,but had little effect in the presence of NADH and Fe(CN)63-.Both hyperand hypoosmotic shock stimulated H+ extrusion.This effect could be totally inhibited by vanadate and DES,but almost unaffected by 8-hydroxyquinoline.It was suggested that H+-ATPase probably played a more important role in H+ extrusion and osmoregulation under the conditions of osmotic shock.
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机译：单细胞卤代藻类杜氏盐藻具有氧化NADH并还原Fe（CN）63-的能力。氧化还原反应在一定程度上受到轻微的高渗休克（2.0mol / L→2.6mol / L NaCl）的刺激，但受到明显的抑制。突然的高渗性休克（2.0mol / L→3.5mol / L NaCl）和低渗性休克（2.0mol / L→1.0mol / L NaCl; 2.0mol / L→0.67mol / L NaCl）。随着藻类细胞对渗透性的适应细胞内甘油的蓄积或腐烂而引起的休克，也恢复了血浆的内膜氧化还原活性。FA和SHAM可促进NADH刺激的O 2吸收。低渗休克提高了藻类细胞的基础呼吸速率，但减弱了NADH，FA的刺激作用另一方面，高渗休克降低了基础呼吸速率，但相对增强了NADH，FA和SHAM的上述作用。NADH抑制藻类细胞的H +挤出并受Fe（CN）63-刺激。钒酸盐和DES可以抑制H +流出，但对NADH和Fe（CN）63-的存在。高渗和低渗休克均刺激了H +的挤出。钒和DES可以完全抑制这种作用，但几乎不受8-羟基喹啉的影响。提示H + -ATPase可能起更重要的作用在渗透性休克条件下在H +挤出和渗透调节中的作用
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