Selenium in Plant Abiotic Stress Tolerance: From Protective Phenotypes to Debated Mechanisms and Practical Applications

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Selenium (Se) exemplifies a striking biological paradox: though non-essential and toxic at high doses, low concentrations enhance plant resilience to drought, salinity, and heavy metals. This review synthesizes peer-reviewed literature from 2000 to 2026 (with a few earlier publications included) retrieved from the Web of Science, Scopus, PubMed, Google Scholar, and CNKI databases, using “selenium,” “abiotic stress tolerance,” “oxidative stress,”and “signaling pathways” as keywords, prioritizing studies that address mechanistic and genetic aspects. We critically evaluate whether Se acts primarily as a direct biochemical participant or as an upstream signaling trigger. Our analysis reveals three key findings: (a) Se predominantly functions as a stress mimic that induces a controlled ROS burst through RBOH-dependent pathways, priming systemic defense through JA/ABA crosstalk and WRKY/MYB/NAC transcription factor networks; (b) for heavy metal stress, this signaling action operates alongside a parallel, concentration-dependent mechanism of direct chemical chelation; and (c) the long-standing question of signaling specificity is addressed by our novel 'sulfur hijacking' hypothesis, proposing that Se generates a unique metabolic signature perceived by an unknown sulfur sensor. We conclude that Se acts primarily as a signaling trigger rather than a direct antioxidant, with its hormetic benefits depending on a narrow, species-specific concentration window. Practically, these insights provide a mechanistic framework for precision Se biofortification, optimizing application rates to balance stress protection against phytotoxicity, and highlight the urgent need for field-validated models that account for soil heterogeneity and multi-stress scenarios.