Many animal species are remarkably resilient to the harmful conditions of hypoxia and reoxygenation, a phenomenon widely observed across many species and environmental settings. The ability to survive oxygen deprivation and reintroduction without significant cellular damage is partially attributed to the upregulation of antioxidants, a strategy termed "Preparation for Oxidative Stress" (POS). The concept of POS is that by producing more antioxidants under hypoxia animals would anticipate the eventual and potentially damaging reintroduction of oxygen. Historically, the specific mechanisms through which POS is activated remained elusive. Over the past decade, significant advancements have been made in understanding POS at a molecular level and in identifying its widespread in the animal kingdom. Notably, a detailed molecular mechanism for the activation of POS under conditions of low oxygen availability has been proposed, emphasizing the role of reactive oxygen species in modulating antioxidant response through redox-sensitive transcription factors. Furthermore, recent research has demonstrated the occurrence of POS in free-ranging animals under completely natural settings, confirming its ecological and physiological relevance. Despite recent advancements, some aspects of POS remain underexplored and should be prioritized in future research. These include the experimental validation of the mechanisms proposed to underlie POS and the assessment of the relevance of POS in multi-stressor scenarios, particularly to understand how organisms cope with combined stressors in fluctuating environments.

Mitochondrial production of O₂^•– and H₂O₂ has been implicated in redox signaling and in the pathogenesis of numerous diseases including cancer, neurodegeneration, and cardiovascular diseases. To understand the exact role of those species, new chemical biology tools for selective and efficient induction of mitochondrial superoxide production are needed. Here, we report the development of a new viologen-based redox cycling agent, mito-diquat (Mito-DQ), capable of inducing targeted mitochondrial O₂^•– production at significantly higher rates as compared to previously reported mito-paraquat (Mito-PQ), a widely used chemical tool to study mitochondria-dependent redox signaling.

Thyroid hormones play an important role in both testis development and spermatogenesis. While hypothyroidism has been known to generally induce metabolic suppression, lower respiration rate, and reduce free radical formation, recent studies reported an increased production of reactive oxygen species (ROS). First line of antioxidant defense in testes is comprised of two isoforms of superoxide dismutase (SOD), CuZnSOD and MnSOD differently localised in cell. This study aimed to investigate the effects of hypothyroidism on the expression, localisation, and activity of these two SOD isoforms during spermatogenesis. Hypothyroidism was induced in two-month-old male Wistar rats by 0.04% methimazole in drinking water for 7, 15, and 21 days, while euthyroid control group drank tap water. CuZnSOD protein expression was decreased after 15 and 21 days while its activity was decreased by 40% in all examined time points of methimazole treatment in comparison to euthyroid control. At the same time, neither MnSOD protein expression nor its activity was changed by treatment. However, cell and stage-specific CuZnSOD and MnSOD immunoexpression in the rat testes were changed in hypothyroidism and may contribute to the altered spermatic characteristics. Our results suggest that changes in CuZnSOD and MnSOD expression play role in redox disbalance leading to hypothyroidism-induced maturation arrest of spermatogenesis.

One of the adaptive features that organisms developed throughout their long natural history is the ability to change the activity of cells, tissues, and organs on a daily, 24-hour, basis. These cyclical changes are synchronized to the external environment through a light-dark regime and internal circadian clock. Daily recurring environmental changes are followed by variations in animal behavior and physiology, which include oscillations in neuroendocrine, metabolic, cardiovascular, and immune functions. By transforming the circadian periodicity of day, artificial light from anthropogenic sources might interfere with organisms leading to a disturbance in hormone levels and physiological stress. In this study, we investigated daily natural variations in the antioxidant system and the effects of artificial light on the redox balance in larvae of tree frogs. We compared antioxidant parameters in tadpoles from the natural day/night cycle (control) with ones exposed to artificial light at night (treatment). The antioxidant response was measured at four time points during 24h (morning, day, evening, and night). Our results showed that only GR activity did not display day/night changes nor was affected by night illumination. For GSH-Px and GST we reported changes in activity at different times of day that were in the same manner for both treatment and control. The highest values were in the morning compared to the other time points. Variation during 24h was also observed for SOD, CAT and GSH. However, exposure to night light affected the pattern and intensity of these parameters compared to the control group. Overall our study suggests that daily differences in metabolic activity can result in variations in the antioxidant system and that the presence of artificial light affects these changes. The disrupted natural rhythm of the antioxidant response may further reflect on other physiological processes and lead to a state of oxidative stress.