Department of Botany and Microbiology, College of Science, King Saud University, Riyadh, 11451, Saudi Arabia.
Department of Botany, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, 110062, India.
Plant Physiol Biochem. 2020 Oct;155:20-34. doi: 10.1016/j.plaphy.2020.07.003. Epub 2020 Jul 20.
Nitric oxide (NO) and hydrogen sulfide (HS), versatile signaling molecules, play multiple roles in plant growth, physiological and biochemical processes under heavy metal stress. However, the mechanisms through which NO in association with endogenous HS mediated hexavalent chromium Cr(VI) toxicity mitigation are still not fully understood. Therefore, we investigated the role of NO and HS in sulfur (S)-assimilation and the effect of NO on endogenous HS, and cysteine (Cys) biosynthesis and maintenance of cellular glutathione (GSH) pool in tomato seedlings under Cr(VI) stress. Cr(VI) toxicity caused an increase in reactive oxygen species (ROS; O and HO) formation and activity of chlorophyll (Chl) degrading enzyme [Chlorophyllase (Chlase)] and decrease in seedlings growth attributes, Chl a and b content, and activity of Chl synthesizing enzyme [δ-aminolevulinic acid dehydratase (δ-ALAD)], gas exchange parameters, S-assimilation, and Cys and HS metabolism. An increase in the content of glycinebetaine (GB), total soluble carbohydrates (TSCs) and total phenols (TPls), and decrease in DNA damage and ROS in NO treated seedlings conferred Cr(VI) toxicity tolerance. Under Cr(VI) toxicity conditions, the inclusion of HS scavenger hypotaurine (HT) in growth medium containing NO validated the role of endogenous HS in S-assimilation, HS and Cys and GSH metabolism by withdrawing activity of enzymes involved in S-assimilation [adenosine 5-phosphosulfatereductase (APS-R), ATP-sulfurylase (ATP-S)], in the biosynthesis of HS [L-cysteine desulfhydrase (L-CD) and D-cysteine desulfhydrase (D-CD)], Cys [O-acetylserin (thiol) lyase (OAST-L)], and GSH [glutamylcysteine synthetase (γ-GCS) and glutathione synthetase (GS)], and in antioxidant system. On the other hand, application of cPTIO [2-(4-32 carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide], a NO scavenger and HT diminished the effect of NO on internal HS levels, Cys and glutathione homeostasis, and S-assimilation, which resulted in poor immunity against oxidative stress induced by Cr(VI) toxicity. The obtained results postulate that NO-induced internal HS conferred tolerance of tomato seedlings to Cr(VI) toxicity and maintained better photosynthesis process and plant growth.
一氧化氮（NO）和硫化氢（HS）是多功能信号分子，在重金属胁迫下的植物生长、生理和生化过程中发挥多种作用。然而，NO 与内源性 HS 介导六价铬 Cr(VI)毒性缓解的机制仍不完全清楚。因此，我们研究了 NO 和 HS 在硫（S）同化中的作用，以及 NO 对内生 HS、半胱氨酸（Cys）生物合成和细胞谷胱甘肽（GSH）库的影响在 Cr(VI)胁迫下的番茄幼苗。Cr(VI)毒性导致活性氧（ROS；O 和 HO）形成和叶绿素（Chl）降解酶[叶绿素酶（Chlase）]活性增加，幼苗生长属性、Chl a 和 b 含量以及 Chl 合成酶[δ-氨基-酮戊酸脱水酶（δ-ALAD）]活性降低，气体交换参数、S 同化以及 Cys 和 HS 代谢。NO 处理的幼苗中甘氨酸甜菜碱（GB）、总可溶性碳水化合物（TSCs）和总酚（TPls）含量增加，DNA 损伤和 ROS 减少，赋予了 Cr(VI)毒性耐受性。在 Cr(VI)毒性条件下，在含有 NO 的生长培养基中加入 HS 清除剂羟乙磺酸（HT），验证了内源性 HS 在 S 同化、HS 和 Cys 和 GSH 代谢中的作用，方法是去除参与 S 同化的酶的活性[腺苷 5-磷酸硫酸酯还原酶（APS-R）、ATP-硫酸化酶（ATP-S）]，在 HS 的生物合成中[L-半胱氨酸脱硫酶（L-CD）和 D-半胱氨酸脱硫酶（D-CD）]、Cys[O-乙酰丝氨酸（硫）裂解酶（OAST-L）]和 GSH[谷氨酰半胱氨酸合成酶（γ-GCS）和谷胱甘肽合成酶（GS）]，以及抗氧化系统。另一方面，应用 NO 清除剂 cPTIO[2-（4-32 羧基苯基）-4,4,5,5-四甲基咪唑啉-1-氧-3-氧化物]和 HT 降低了 NO 对内源 HS 水平、Cys 和谷胱甘肽稳态以及 S 同化的影响，导致对 Cr(VI)毒性诱导的氧化应激的免疫力下降。研究结果表明，NO 诱导的内源性 HS 赋予了番茄幼苗对 Cr(VI)毒性的耐受性，并维持了更好的光合作用过程和植物生长。
