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<p>5-aminolevulinic acid (ALA) is known to alleviate cadmium (Cd)-induced damage. However, the underlying signaling mechanisms remain unclear, particularly those of nitric oxide (NO) and hydrogen sulfide (H<sub>2</sub>S). To fill this gap, the present study explores the contribution of NO and H₂S to 5-ALA-mediated Cd tolerance in chickpea (<i>Cicer arietinum</i>) seedlings. Chickpea seeds were primed with ALA (10 mg L<sup>− 1</sup>) before exposure to 200 µM Cd or pretreated with inhibitors of nitric oxide (NOi) or hydrogen sulfide (H<sub>2</sub>Si) biosynthesis. During germination, pretreated seeds with inhibitors were further exposed to sodium nitroprusside (SNP, an NO donor) or NaHS (an H<sub>2</sub>S donor). Cadmium stress inhibited seedling growth and disrupted cell membrane structure, as indicated by increased malondialdehyde (MDA) accumulation and elevated lipoxygenase (LOX) activity. Seed priming with ALA mitigated Cd-induced growth inhibition and reduced Cd accumulation by 41%. Moreover, ALA protected cell membrane integrity, as evidenced by a 1.8-fold decrease in MDA content. Additionally, ALA exacerbated the Cd-elicited increase in NO and H<sub>2</sub>S accumulation and stimulated the activities of nitrate reductase (NR), nitrite reductase (NiR), and L-cysteine desulfhydrase (LCD). However, pretreatment of seeds with NOi or H<sub>2</sub>Si before ALA priming abolished its protective effects against Cd toxicity. The subsequent application of SNP and NaHS restored the beneficial role of ALA, counteracting the inhibitory impact of NOi and H<sub>2</sub>Si. These findings suggest that NO and H<sub>2</sub>S are crucial effectors in ALA-mediated protection against Cd stress.</p>

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Interplay Between Hydrogen Sulfide and Nitric Oxide Signaling Pathways in 5-Aminolevulinic Acid-Mediated Alleviation of Cadmium Stress in Chickpea Seedlings

  • 期刊论文

  • 发表日期：

    2025年6月13日

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  • Lamia Sakouhi,
  • Oussama Kharbech,
  • Marwa Boutar,
  • Muhammad Hussaan,
  • Yoshiyuki Murata,
  • Abdelilah Chaoui

摘要

5-aminolevulinic acid (ALA) is known to alleviate cadmium (Cd)-induced damage. However, the underlying signaling mechanisms remain unclear, particularly those of nitric oxide (NO) and hydrogen sulfide (H2S). To fill this gap, the present study explores the contribution of NO and H₂S to 5-ALA-mediated Cd tolerance in chickpea (Cicer arietinum) seedlings. Chickpea seeds were primed with ALA (10 mg L− 1) before exposure to 200 µM Cd or pretreated with inhibitors of nitric oxide (NOi) or hydrogen sulfide (H2Si) biosynthesis. During germination, pretreated seeds with inhibitors were further exposed to sodium nitroprusside (SNP, an NO donor) or NaHS (an H2S donor). Cadmium stress inhibited seedling growth and disrupted cell membrane structure, as indicated by increased malondialdehyde (MDA) accumulation and elevated lipoxygenase (LOX) activity. Seed priming with ALA mitigated Cd-induced growth inhibition and reduced Cd accumulation by 41%. Moreover, ALA protected cell membrane integrity, as evidenced by a 1.8-fold decrease in MDA content. Additionally, ALA exacerbated the Cd-elicited increase in NO and H2S accumulation and stimulated the activities of nitrate reductase (NR), nitrite reductase (NiR), and L-cysteine desulfhydrase (LCD). However, pretreatment of seeds with NOi or H2Si before ALA priming abolished its protective effects against Cd toxicity. The subsequent application of SNP and NaHS restored the beneficial role of ALA, counteracting the inhibitory impact of NOi and H2Si. These findings suggest that NO and H2S are crucial effectors in ALA-mediated protection against Cd stress.