OXIDATIVE STRESS PHYSIOLOGY IN ANIMALS: REACTIVE OXYGEN SPECIES AS A CENTRAL MEDIATOR OF THE RESPONSE TO ENVIRONMENTAL STRESSORS

Abstract

Aerobic life is, in a sense, a bargain. Oxygen fuels the energy metabolism that animals depend upon, yet the very chemistry that extracts energy from nutrients also leaks partially reduced oxygen species back into the cell. These reactive oxygen species (ROS), together with reactive nitrogen species, sit at the heart of a continuous physiological balancing act: at low and tightly controlled levels they serve as second messengers and help shape cellular signalling, whereas when their generation outpaces the antioxidant machinery they begin to damage lipids, proteins and nucleic acids. This imbalance, termed oxidative stress, has become over the last three decades one of the more useful organising concepts in comparative and environmental physiology. Here we argue that oxidative stress is best understood not as a disease state but as a central mediator that translates a broad range of environmental challenges — thermal extremes, fluctuating oxygen, shifting salinity, food limitation and chemical pollution — into integrated physiological, life-history and fitness outcomes. We summarise the principal sources of ROS in animal tissues, the enzymatic and non-enzymatic defences that hold them in check, and the redox-sensitive signalling networks, the Keap1–Nrf2 axis in particular, that couple perturbation to adaptive gene expression. We then examine how individual stressors modulate oxidative balance, why the resulting responses are so often context-dependent, and how phenomena such as hormesis, preparation for oxidative stress and cross-tolerance complicate any simple dose–response logic. We close by highlighting persistent methodological problems and several directions that, in our view, deserve closer attention.