Gianluca Fasciolo

In recent years, interest in the impact of environmental pollutants on the ecosystem has increased significantly, with particular attention being paid to the relationship between climate change and the aquatic world. This is because increasing pollution is causing fundamental changes to the welfare of animals and the marine ecosystem. A primary focus is on the impact of microplastics (MPs) and nanoplastics (NPs), as evidenced by our bibliometric network analysis (BNA). However, while research is focused on the accumulation of these pollutants in aquatic organisms, their effects on redox homeostasis are still seldom discussed despite the role played by reactive oxygen species and mitochondrial well-being in maintaining an optimal state of health. However, some scientific evidence suggests that the accumulation of MPs and NPs in organisms at the base of the trophic chain can cause a transfer of these substances towards more complex organisms, reaching humans through the consumption of aquatic fauna as food. Therefore, in this review, we have tried to discuss the effects of these substances on oxidative stress in aquatic organisms, even if studies in this regard are still scarce.

Aerobic organisms use molecular oxygen in several reactions, including those in which the oxidation of substrate molecules is coupled to oxygen reduction to produce large amounts of metabolic energy. The utilization of oxygen is associated with the production of ROS, which can damage biological macromolecules but also act as signaling molecules, regulating numerous cellular processes. Mitochondria are the cellular sites where most of the metabolic energy is produced and perform numerous physiological functions by acting as regulatory hubs of cellular metabolism. They retain the remnants of their bacterial ancestors, including an independent genome that encodes part of their protein equipment; they have an accurate quality control system; and control of cellular functions also depends on communication with the nucleus. During aging, mitochondria can undergo dysfunctions, some of which are mediated by ROS. In this review, after a description of how aging affects the mitochondrial quality and quality control system and the involvement of mitochondria in inflammation, we report information on how vitamin E, the main fat-soluble antioxidant, can protect mitochondria from age-related changes. The information in this regard is scarce and limited to some tissues and some aspects of mitochondrial alterations in aging. Improving knowledge of the effects of vitamin E on aging is essential to defining an optimal strategy for healthy aging.