Aquatic ecosystems are exposed to numerous chemical pollutants due to increasing industrialization, intensive agricultural activities, and urbanization. These pollutants often produce sublethal and chronic toxic effects in organisms through low concentrations and long-term exposures, rather than causing acute and lethal effects. Recent studies have revealed that oxidative stress mechanisms play a central role in understanding the effects of such sublethal exposures. This review article addresses the mechanisms by which inorganic and organic chemical pollutants in aquatic environments cause toxicity through oxidative stress, taking a holistic approach within the context of chemical structure-reactivity properties and cellular redox balance. Cellular damage processes such as increased reactive oxygen species (ROS), antioxidant defense system responses, lipid peroxidation, protein oxidation, DNA damage, and mitochondrial dysfunction are discussed in detail. Furthermore, the study evaluated how redox-sensitive signaling pathways such as Nrf2/Keap1, MAPK, NF-κB, PPAR, and AhR shape toxicity responses under sublethal exposure conditions. The review highlighted the long-term effects of chronic and low-dose exposures on growth, immunity, energy metabolism, and reproductive performance, as well as the population and ecosystem-level implications of these effects. Finally, the contributions of oxidative stress-based biomarkers and mechanistic toxicity approaches to environmental risk assessments beyond classical acute toxicity testing were discussed. In this context, the study aims to contribute to the development of more sensitive, predictive, and scientifically based assessment strategies for the conservation of aquatic ecosystems.
Uzun et al. (Sun,) studied this question.