The aim of this manuscript was to investigate the role of calcium compounds, viz., Ca(OH) 2 , Ca(NO 3 ) 2 , and CaCl 2 (each used at 0.3 mM and 0.5 mM concentration) as seed priming agents to ameliorate fluoride toxicity in rice. The stressed seedlings exhibited high fluoride bioaccumulation, severe growth retardation, and cellular damages. Calcium compounds improved plant performance by increasing seed germination, seedling biomass, and root and shoot length, avoiding chlorophyll degeneration and leakage of electrolytes, along with lowering the levels of malondialdehdye, H 2 O 2 , and endogenous fluoride. Calcium-regulated defence was mediated by proline synthesised due to increased Δ 1 -pyrroline 5-carboxylate synthetase ( P5CS ) and lowered proline dehydrogenase ( PDH ) expression, and glycine betaine synthesised due to betaine aldehyde dehydrogenase 1 ( BADH1 ) expression. While the stress-mediated lowering of carotenoids and total phenolics was relieved by calcium priming, stress-enhanced flavonoids and ascorbic acid content was restored to the normal condition, along with releasing the fluoride-induced inhibition of ascorbic acid oxidase (AAO) activity. The activities of antioxidant enzymes like catalase, guaiacol peroxidase, and superoxide dismutase, and the expression of catalase and superoxide dismutase genes were also affected by calcium priming. The elevated endogenous calcium level, brought about by priming, enhanced the expression of genes related to calcium signalling pathway, particularly the calcineurin-B-like 10 ( CBL10 ) gene. Ca(OH) 2 (0.3 mM) appeared to be the most efficient of all the three priming agents. Overall, the present work highlighted the efficacy of calcium compounds as priming agents in abrogating fluoride toxicity in rice.

中文翻译：

---

用钙化合物引发种子通过上调籼稻品种的防御途径来消除氟化物诱导的氧化应激

本手稿的目的是研究钙化合物的作用，即 Ca(OH) 2 、Ca(NO 3 ) 2 和 CaCl 2（各自以 0.3 mM 和 0.5 mM 浓度使用）作为种子引发剂以改善大米中的氟中毒。受胁迫的幼苗表现出高氟生物蓄积性、严重的生长迟缓和细胞损伤。钙化合物通过增加种子发芽、幼苗生物量、根和芽长度，避免叶绿素变性和电解质泄漏，同时降低丙二醛、H 2 O 2 和内源性氟化物的水平来改善植物性能。由于Δ1-吡咯啉5-羧酸合成酶（P5CS）增加和脯氨酸脱氢酶（PDH）表达降低，脯氨酸合成介导钙调节防御，由于甜菜碱醛脱氢酶 1 (BADH1) 表达而合成的甘氨酸甜菜碱。虽然压力介导的类胡萝卜素和总酚类物质的降低被钙引发缓解，但压力增强的黄酮类化合物和抗坏血酸含量恢复到正常状态，同时释放氟化物诱导的抗坏血酸氧化酶 (AAO) 活性抑制。过氧化氢酶、愈创木酚过氧化物酶和超氧化物歧化酶等抗氧化酶的活性以及过氧化氢酶和超氧化物歧化酶基因的表达也受钙引发的影响。引发引起的内源性钙水平升高，增强了与钙信号通路相关的基因的表达，尤其是钙调神经磷酸酶-B 样 10 (CBL10) 基因。Ca(OH) 2 (0.3 mM) 似乎是所有三种引发剂中最有效的。