Heterologous GSNOR expression modulates nitric oxide and glutathione redox to differentially shape plant responses to herbicides.

Redox and nitric oxide (NO) signaling are central to plant responses to herbicides, yet whether strengthening NO-redox buffering improves tolerance remains unresolved. We generated Arabidopsis thaliana lines overexpressing the bacterial S-nitrosoglutathione reductase (GSNOR) gene FrmA, alone (FrmAOE) or together with its operon partner (FrmA/BOE), and compared responses to four herbicides with distinct modes of action under controlled laboratory conditions. Under atrazine (a photosystem II inhibitor), transgenic plants exhibited improved oxidative tolerance: glutathione (GSH) increased by 127 %, NO decreased by 38 %, and PSII performance and biomass loss were mitigated. In contrast, under imazethapyr and glufosinate (which inhibit branched-chain amino acid synthesis and glutamine synthetase, respectively), NO increased by up to 135 %, GSH declined by more than 50 %, and ammonium accumulated approximately fourfold, accompanying PSII impairment and metabolic disruption. These results from this Arabidopsis system suggest that GSNOR overexpression is associated with fortification of redox buffering under ROS-dominant stress but aggravates toxicity when nitrogen metabolism is targeted, revealing a stress-specific trade-off. We outline a framework in which engineered NO-redox buffering is beneficial when oxidative load predominates, yet may risk destabilizing nitrogen homeostasis under amino-nitrogen pathway inhibition. This conditionality clarifies when redox engineering is likely to improve herbicide resilience in plants and outlines translational boundaries for deploying GSNOR-based strategies in crop protection.

• Publication year

  2026

• Venue

  Journal of Hazardous Materials

• Publication date

  2026-01-26

• Fields of study

  Biology, Medicine, Environmental Science

• Identifiers
  DOI 10.1016/j.jhazmat.2026.141261PMID 41604923
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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