Redox Balance and Repair Fidelity Govern the Continuum of Radiation Effects in Plants

Abstract

Ionizing radiation exerts both beneficial and deleterious effects on plants, depending on dose, rate and physiological state. Historically, two distinct research traditions have emerged: the genetic paradigm, focused on high-dose mutagenesis for breeding, and the physiological paradigm, focused on low-dose stimulation known as radiohormesis. Although often treated as independent, both derive from the same underlying radiochemical and biochemical chain of events: energy deposition, reactive oxygen species (ROS) formation, antioxidant response and repair fidelity. This paper proposes a unifying theoretical framework in which physiological, mutagenic and sterilizing outcomes appear as continuous manifestations of a single dynamic balance between ROS generation and repair throughput. A minimal kinetic model is introduced, coupling ROS accumulation, inducible antioxidant capacity and cumulative lesion load. From these relations, a dimensionless repair challenge number (=) is derived, serving as the control parameter that orders the transition between adaptive, mutagenic and lethal regimes. Building on this kinetic foundation, we formulate an analytical dose-response model, E(D), intended as a phenomenological summary of the redox-repair balance. The formulation reproduces a hormetic rise at low doses and adamage-dominated decline at higher doses. Analytical results suggest the existence of an interior maximum and, under standard unimodality assumptions, its operational uniqueness corresponding to optimal physiological response, while a fidelity function F(D) links this maximum to the onset of mutational inaccuracy. Together, these relations help clarify why small variations in dose, rate or genotype can shift outcomes from stimulation to inhibition or mutation.