Organ-specific redox and trace element modulation and hematological adaptation following hyperbaric oxygenation and...

Oxidative stress represents an imbalance between the production of reactive oxygen species and the capacity of antioxidant defense systems to neutralize them. Both acute physical activity and hyperbaric oxygen exposure can influence redox homeostasis; however, their combined effects on systemic and tissue-specific oxidative status and trace element balance remain insufficiently understood. The aim of this study was to investigate the effects of hyperbaric oxygen preconditioning on oxidative stress parameters, antioxidant defense mechanisms, and elemental homeostasis following acute physical activity in previously untrained rats.

Male Wistar rats were randomly assigned to four groups: control, physical activity (PA), hyperbaric oxygenation (HBO), and PA following HBO exposure (HBO + PA).

Across most measured parameters, no significant interaction between HBO and PA was detected, suggesting that their effects act largely independently. Instead, several significant main effects were identified. In particular, HBO increased erythrocyte count, hemoglobin concentration, and hematocrit, while erythrocyte indices remained unchanged, and were accompanied by increased total protein, albumin, and urea levels. HBO exerted a significant main effect on WBC count, while both HBO and PA were associated with lower lymphocyte counts. Systemic oxidative stress markers showed minimal alterations. An exception was catalase activity, which exhibited significant interaction. Nevertheless, distinct tissue-specific responses were observed. HBO was associated with increased lipid peroxidation in liver tissue, whereas in kidney tissue, HBO reduced lipid peroxidation and attenuated PA-associated depletion of sulfhydryl groups, highlighting organ-dependent redox modulation. Elemental findings further confirmed the predominance of main effects. In kidney tissue, HBO was linked to lower potassium, magnesium, phosphorus, zinc and lead levels, while PA was associated with lower iron and arsenic concentrations, and both interventions contributed to decreased sodium and mercury levels. In liver tissue, both PA and HBO were associated with reduced sodium levels, whereas HBO was associated with lower potassium and PA with higher magnesium concentrations. Phosphorus, manganese, copper, cobalt, and selenium demonstrated significant main effects; however, post hoc analyses did not reveal specific differences between individual experimental groups.

Collectively, these findings suggest that short-term HBO and acute PA are associated with distinct organ-specific responses in redox balance and elemental homeostasis, predominantly through independent rather than interactive mechanisms.