Ranjan Plant Physiology and Biochemistry Laboratory, Department of Botany, University of Allahabad, Prayagraj, 211002, India.
J Plant Res. 2024 May;137(3):521-543. doi: 10.1007/s10265-024-01530-7. Epub 2024 Mar 9.
The present study examined the regulatory mechanism of hydrogen sulfide (HS) and nitric oxide (NO) in nickel (Ni) stressed cyanobacteria viz., Nostoc muscorum and Anabaena sp. by analyzing growth, photosynthetic pigments, biochemical components (protein and carbohydrate), exopolysaccharides (EPS), inorganic nitrogen content, and activity of enzymes comprised in nitrogen metabolism and Ni accumulation. The 1 µM Ni substantially diminished growth by 18% and 22% in N. muscorum and Anabaena sp. respectively, along with declining the pigment contents (Chl a/Car ratio and phycobiliproteins), and biochemical components. It also exerted negative impacts on inorganic uptake of nitrate and nitrite contents; nitrate reductase and nitrite reductase; and ammonium assimilating enzymes (glutamine synthetase, glutamate synthase, and glutamate dehydrogenase exhibited a reverse trend) activities. Nonetheless, the adverse impact of Ni can be mitigated through the exogenous supplementation of NaHS [sodium hydrosulfide (8 µM); HS donor] and SNP [sodium nitroprusside (10 µM); NO donor] which showed substantial improvement on growth, pigments, nitrogen metabolism, and EPS layer and noticeably occurred as a consequence of a substantial reduction in Ni accumulation content which minimized the toxicity effects. The accumulation of Ni on both the cyanobacterial cell surface (EPS layer) are confirmed by the SEM-EDX analysis. Further, the addition of NO scavenger (PTIO; 20 µM) and inhibitor of NO (L-NAME; 100 µM); and HS scavenger (HT; 20 µM) and HS inhibitor (PAG; 50 µM) reversed the positive responses of HS and NO and damages were more prominent under Ni stress thereby, suggesting the downstream signaling of HS on NO-mediated alleviation. Thus, this study concludes the crosstalk mechanism of HS and NO in the mitigation of Ni-induced toxicity in rice field cyanobacteria.
本研究通过分析生长、光合色素、生化成分（蛋白质和碳水化合物）、胞外多糖（EPS）、无机氮含量以及氮代谢和镍积累相关酶的活性，研究了硫化氢（HS）和一氧化氮（NO）在镍（Ni）胁迫下蓝藻 Nostoc muscorum 和 Anabaena sp.中的调控机制。1µM 的 Ni 显著抑制了 N. muscorum 和 Anabaena sp. 的生长，分别降低了 18%和 22%，同时降低了色素含量（Chl a/Car 比和藻胆蛋白）和生化成分。它还对硝酸盐和亚硝酸盐的无机摄取、硝酸还原酶和亚硝酸还原酶以及铵同化酶（谷氨酰胺合成酶、谷氨酸合酶和谷氨酸脱氢酶表现出相反的趋势）的活性产生负面影响。然而，通过外源添加 NaHS [氢硫化钠（8µM）；HS 供体]和 SNP [硝普酸钠（10µM）；NO 供体]可以减轻 Ni 的不利影响，这两种物质显著改善了生长、色素、氮代谢和 EPS 层，并由于 Ni 积累含量的显著降低，从而减轻了毒性作用。SEM-EDX 分析证实了 Ni 积累在蓝藻细胞表面（EPS 层）上。此外，添加 NO 清除剂（PTIO；20µM）和 NO 抑制剂（L-NAME；100µM）；以及 HS 清除剂（HT；20µM）和 HS 抑制剂（PAG；50µM）逆转了 HS 和 NO 的正响应，并且在 Ni 胁迫下损伤更为明显，这表明 HS 在 NO 介导的缓解作用中的下游信号转导。因此，本研究得出结论，HS 和 NO 之间的串扰机制可以减轻稻田蓝藻中 Ni 诱导的毒性。
