Present investigation reports the role of calcium (Ca²⁺) and hydrogen sulfide (H₂S) crosstalk associated with Vigna radiata seedlings subjected to K⁺ deficient conditions under short-term (24 h) and long-term (72 h) NaCl stress. Perusal of the data reveals that under short-term NaCl stress an initial decline in K⁺ level led to the elevation in Ca²⁺ and H₂S levels along with improvement in antioxidant system and reduction in reactive oxygen species (ROS) production. Under long-term NaCl stress a further decline in K⁺ content was deleterious that led to a lower K⁺/Na⁺ ratio. This was followed by reduction in antioxidant system along with excessive accumulation of ROS and methylglyoxal content, and increased membrane damage. However, supplementation of the seedling roots with Ca²⁺ enhanced biosynthesis of H₂S through enhancing cysteine pool. The present findings suggest that synergistic action of Ca²⁺ and H₂S induced the activity of H⁺-ATPase that created H⁺ gradient which in turn induced Na⁺/H⁺ antiport system that accelerated K⁺ influx and Na⁺ efflux. All of these together contributed to a higher K⁺/Na⁺ ratio, activation of antioxidative defense system, and maintenance of redox homeostasis and membrane integrity in Ca²⁺-supplemented stressed seedlings. Role of Ca²⁺ and H₂S in the regulation of Na⁺/H⁺ antiport system was validated by the use of sodium orthovanadate (plasma membrane H⁺-ATPase inhibitor), tetraethylammonium chloride (K⁺ channel blocker), and amiloride (Na⁺/H⁺ antiporter inhibitor). Application of Ca²⁺-chelator EGTA (ethylene glycol-bis(b-aminoethylether)-N,N,Nʹ,Nʹ-tetraacetic acid) and H₂S scavenger hypotaurine abolished the effect of Ca²⁺, suggesting the involvement of Ca²⁺ and H₂S in the alleviation of NaCl stress. Moreover, use of EGTA and HT also substantiates the downstream functioning of H₂S during Ca²⁺-mediated regulation of plant adaptive responses to NaCl stress. To sum up, present findings reveal the association of Ca²⁺ and H₂S signaling in the regulation of ion homeostasis and antioxidant defense during K⁺-deficient NaCl stress.

本调查报告钙（Ca的作用²⁺）和硫化氢（H ₂ S）串扰相关的绿豆进行至K苗⁺短期（24小时）和长期（72小时）盐胁迫下缺乏条件。数据的统计显示，在短期NaCl胁迫下，K ⁺含量的初始下降导致Ca ²⁺和H ₂ S含量升高，同时抗氧化剂系统得到改善，活性氧（ROS）产量降低。在长期的NaCl胁迫下，K ⁺含量进一步下降是有害的，导致K ⁺ / Na ^+降低。比。其次是减少抗氧化剂系统，以及过多的ROS和甲基乙二醛含量积聚，并增加膜损伤。然而，通过增强半胱氨酸池，用Ca ²⁺补充幼苗根可以增强H ₂ S的生物合成。目前的发现表明，Ca ²⁺和H ₂ S的协同作用诱导了H ⁺ -ATPase的活性，从而产生了H ⁺梯度，进而诱导了Na ⁺ / H ⁺反转运系统，从而加速了K ^+内流和Na ⁺外排。所有这些共同导致更高的K ⁺ / Na ⁺Ca ²⁺胁迫的幼苗中的比例，抗氧化防御系统的活化以及氧化还原稳态和膜完整性的维持。通过使用原钒酸钠（质膜H ⁺ -ATPase抑制剂），氯化四乙铵（K ⁺通道阻滞剂）和阿米洛利（以下简称Amir）验证了Ca ²⁺和H ₂ S在Na ⁺ / H ⁺反向转运系统调节中的作用。Na ⁺ / H ⁺反向转运抑制剂）。Ca 2 ^+-螯合剂EGTA（乙二醇-双（b-氨基乙基醚）-N，N，Nʹ，Nʹ-四乙酸）和H _2的应用S清除剂低牛磺酸消除了Ca ²⁺的作用，表明Ca ²⁺和H ₂ S参与了NaCl胁迫的缓解。此外，EGTA和HT的使用还证实了Ca ²⁺介导的植物对NaCl胁迫的适应性调节过程中H ₂ S的下游功能。综上所述，目前的发现揭示了Ca ²⁺和H ₂ S信号传导在缺钾⁺ NaCl胁迫期间调节离子稳态和抗氧化防御的关联。