Reactive oxygen species (ROS) in insects are commonly discussed as if they occupy a single continuum from low, beneficial signaling to high, damaging oxidative stress. Recent mechanistic studies instead indicate that biological meaning depends on where reactive species originate, where they act, how long they persist, the physiological state in which they arise, and the strength of evidence linking an oxidation event to function. This state-of-the-art review integrates redox regulation across immunity, aging, environmental stress, metabolism, antioxidant defense, and repair while preserving these distinctions. Insect studies show that hydrogen peroxide and mitochondrial ROS can transmit information in neural, regenerative, immune, developmental, and stress-response settings, whereas similar oxidant accumulation can also compromise barrier integrity, amplify inflammatory injury, or accompany reproductive decline. Antioxidant proteins likewise cannot be treated only as scavengers: thioredoxin, peroxiredoxin, glutathione-related enzymes, and redox-sensitive transcriptional systems can participate in signaling, detoxification, metabolism, autophagy, and repair. We therefore advance a proposed context-gated interpretation in which source identity, spatial compartment, temporal regime, biological state, and inference strength jointly determine what a redox measurement can support. The framework separates signaling from damage, acute response from evolutionary adaptation, and molecular perturbation from organismal consequence. Its main implication is methodological: insect redox biology will progress most reliably when chemically and spatially resolved measurements are connected to perturbation, rescue, identified molecular targets, and explicitly bounded organismal outcomes.
