Overview
Plants and animals follow the same excitation to redox architecture. Both kingdoms produce reactive oxygen species through stress and through the presence of persistent foreign objects. Each system uses calcium linked pathways to generate the same oxidant species, and each system produces the same biological outcomes when the load becomes too high.
Stress of every type increases calcium signaling in both kingdoms. In animals, psychological, environmental, thermal, and metabolic stress increase glutamate receptor activity, raise calcium influx, and elevate mitochondrial production of superoxide and hydrogen peroxide (Khan et al., 2024). In plants, drought, cold, heat, salinity, and mechanical injury activate GLR channels and RBOH enzymes which convert NADPH into superoxide and hydrogen peroxide (Marino et al., 2012). The result is a shared baseline of stress induced oxidative activity that follows the same biochemical rules in both kingdoms.
Persistent foreign objects create the second path and the parallel is exact. In animals, macrophages surround objects that cannot be removed such as particulates, bacteria, or environmental irritants. They attempt to engulf the object repeatedly, and this containment effort becomes a stable ring of activated cells that produces continuous reactive oxygen species. This activation drives the kynurenine pathway toward quinolinic acid which is a ligand that amplifies NMDA receptor activity and increases calcium influx.
In plants, insects, nematodes, microbes, or injected compounds remain embedded and cannot be removed. The surrounding tissue forms a gall that encloses the object, which creates a structural containment ring that directly parallels animal inflammation. Gall tissue produces elevated auxin which increases the activation rate of GLR channels and amplifies RBOH activity. This increases calcium throughput and increases reactive oxygen species production exactly like quinolinic acid does in animals.
Auxin in plants and quinolinic acid in animals therefore act as ligand amplifiers. They increase the frequency of activation in cells near the foreign object and accelerate the containment effort. Each ligand increases calcium signaling, increases reactive oxygen species, and pushes the local tissue toward oxidative strain.
The cell then enters one of two possible outcomes which determine all non genetic plant and animal disease. If the cell does not switch into glycolysis when its oxidative load becomes too high, reactive oxygen species continue to rise beyond its repair capacity. This produces degeneration. Neurons degenerate through excitotoxic collapse, immune cells lock into chronic activation, muscle cells fail from oxidation, and epithelial and vascular cells break down. In plants, leaves, stems, roots, and vascular bundles show collapse of redox systems and cell death. Most non genetic human disease and a large part of plant disease follow this path.
If the cell does switch into glycolysis it reduces mitochondrial reactive oxygen species and survives, but glycolysis creates a survival program that increases growth pressure. If this program persists it becomes locked by methylation. In animals this becomes the early tumor environment. In plants this becomes the hypergrowth phase of a gall. Tumors and galls are therefore parallel outcomes that emerge only after the glycolytic switch and after the survival program becomes stabilized.
Stress therefore pushes both kingdoms through the same sequence. Stress increases calcium signaling. Calcium increases reactive oxygen species. Reactive oxygen species force a threshold choice. Failure to switch to glycolysis produces degeneration. Switching to glycolysis produces survival but risks methylation driven hypergrowth. The location of the affected tissue determines the visible disorder.
Transgenerational inheritance follows the same symmetry. In animals, stress methylates NR3C1, FKBP5, HSD11B2, and related loci which alter receptor expression and increase excitability in the next generation. Hypomethylation at excitatory genes becomes common in offspring of stressed parents. In plants, drought and salt stress produce hypomethylation at stress signaling loci, open chromatin, and primed activation states that persist in the next generation. The mechanism is the same. Stress induced methylation in the parent shifts the excitatory threshold in the offspring.
This establishes a single conserved excitatory redox system across plants and animals. Stress and foreign object containment activate the same ligand pathways. Calcium and reactive oxygen species follow identical kinetics. Cells enter degeneration or glycolytic survival through the same rules. Hypergrowth or death emerges from the same oxidative threshold. Inheritance patterns preserve these states in both kingdoms. The architecture is unified and continuous.
GLR and Glutamate Receptor Parallels
GLR channels in plants and NMDA and AMPA receptors in animals are functional equivalents that control calcium entry and determine the magnitude of reactive oxygen species production. Plant GLRs regulate hydrogen peroxide signaling during cold and salt stress and maintain redox balance during acclimation (Li et al., 2019). GLR mediated nitric oxide signaling also preserves antioxidant function under salt stress (Gokce et al., 2024).
In animals, NMDA and AMPA receptor activation increases calcium influx, accelerates mitochondrial respiration, and increases superoxide and hydrogen peroxide production during excitatory states (Khan et al., 2024).
Both systems use the same excitation mechanics to produce reactive oxygen species.
RBOH and Mitochondrial ROS Amplification
Plants and animals use similar machinery to amplify reactive oxygen species once calcium rises. Plants use RBOH enzymes which convert NADPH into superoxide and hydrogen peroxide. These enzymes are activated by calcium and phosphorylation and act as core amplifiers in every major stress pathway (Marino et al., 2012). Their regulation of oxidative bursts is documented across all major plant stress responses (Suzuki et al., 2011).
Animals use mitochondria and NADPH oxidases. Calcium increases electron flow and increases mitochondrial reactive oxygen species through the same chemistry that defines RBOH production in plants (Wu et al., 2025).
The parallel is exact at the level of oxidant species and activation logic.
Beneficial ROS and the Threshold to Injury
Reactive oxygen species regulate development, patterning, and stress adaptation in both kingdoms (Noctor et al., 2018). The same species become harmful when their levels exceed antioxidant capacity. Lipid peroxidation, protein oxidation, DNA damage, chloroplast injury, and mitochondrial collapse occur through the same biochemical reactions in both plants and animals (Sharma et al., 2012); (Das and Roychoudhury, 2014). Environmental stress pushes plants beyond this threshold (Hasanuzzaman et al., 2020); (Xie et al., 2019). Psychological, metabolic, and inflammatory stress do the same in animals and in transgenerational models such as the duck lineage study where parental stress altered glucocorticoid physiology and excitatory load in offspring (Oluwagbenga et al., 2025).
The oxidative threshold that separates adaptation from injury is shared across both kingdoms.
Ligand Amplification by Auxin and Quinolinic Acid
Auxin in plants and quinolinic acid in animals act as ligand amplifiers that increase excitatory pressure during foreign object containment. In animals, chronic inflammation drives quinolinic acid synthesis which activates NMDA receptors, increases calcium influx, and elevates reactive oxygen species production. In plants, galling increases auxin concentration which increases GLR activation and stimulates RBOH enzymes, creating the same chronic excitatory environment (Gokce et al., 2024).
Each ligand increases activation frequency and increases the energy available to containment cells. This accelerates the containment effort and increases oxidative load.
If the load becomes too high the cell faces the same choice in animals and in plants. It can shift into glycolysis and survive or it can fail to shift and progress to oxidative injury and death.
Glycolytic Shift in Both Kingdoms
When reactive oxygen species exceed mitochondrial tolerance the cell moves toward glycolysis to avoid oxidative collapse. In animals this produces the early tumor environment. In plants this appears in the hypergrowth phase of galled tissue. Each environment is built on the same survival program and each becomes stabilized by methylation when the program persists (Hasanuzzaman et al., 2020).
If the glycolytic mode persists it becomes epigenetically locked. This converts survival into hypergrowth. Tumors and galls are therefore parallel structures that form only after the glycolytic shift and only after methylation stabilizes the state.
Programmed Cell Death Parallels
When survival fails, both kingdoms initiate reactive oxygen species linked cell death. High reactive oxygen species oxidize cardiolipin, collapse mitochondrial control, and permeabilize the outer membrane. In plants this causes cytochrome c to move into the cytosol where it initiates programmed cell death pathways (Petrov et al., 2015). Reviews confirm cytochrome c release as a conserved death signal in plant cells (Karuppanapandian et al., 2011).
Animals follow the same sequence. Excitotoxic overload releases cytochrome c into the cytosol which activates apoptotic machinery (Wu et al., 2025).
The mitochondrial death checkpoint is therefore identical in plants and animals.
Unified View
Every component of this architecture is shared across both kingdoms. Stress increases calcium signaling and reactive oxygen species in the same way. Foreign object containment creates the same ligand reinforced excitatory rings. Auxin and quinolinic acid increase activation frequency and increase oxidant production. Reactive oxygen species force the same threshold decision in every cell. Failure to switch into glycolysis produces degeneration and death. Switching into glycolysis produces survival but risks methylation driven hypergrowth. Tumors and galls follow the same logic. Transgenerational inheritance preserves these excitatory states in both plants and animals.
The excitatory redox system is therefore conserved across the plant and animal kingdoms and explains the major non genetic disease states of both.