Introduction
Reduced dissolved oxygen availability is an increasing challenge for salmonid aquaculture, particularly under climate change scenarios where rising water temperatures decrease oxygen solubility while increasing metabolic demand (Johnston et al., 2025). Chronic hypoxia can impair growth and feed utilization and induce physiological disturbances associated with oxidative stress and activation of stress-response pathways (Lushchak, 2011; Magnoni et al., 2018). Nutritional strategies supporting antioxidant defenses and maintaining redox homeostasis are therefore receiving growing attention (Ciji and Akhtar, 2021). Antarctic krill meal (KM) is a functional ingredient rich in antioxidant compounds, including astaxanthin, selenium and vitamins, and has been associated with beneficial effects on fish performance and health (Kaur et al., 2022). However, its role in modulating physiological stress and redox responses under hypoxic conditions remains poorly documented. Therefore, this study investigated the effects of dietary KM supplementation on stress-related and antioxidant responses of juvenile rainbow trout exposed to chronic hypoxia.
Materials and methods
Juvenile rainbow trout (37 ± 1 g) were fed a control diet (CTRL) or diets supplemented with 5% (KM5), 7.5% (KM7) or 10% (KM10) krill meal for 12 weeks under normoxic conditions. Fish were subsequently exposed to chronic hypoxia (5.9–6.5 mg/L dissolved oxygen) for 3 weeks while continuing to receive their respective diets. Plasma stress indicators (cortisol and glucose), total antioxidant capacity (TAC), hepatic glutathione redox status and expression of antioxidant- and hypoxia-related genes were assessed. Effects of diet and rearing condition were analysed by ANOVA.
Results and discussion
Figure 1. Plasma cortisol and total antioxidant capacity of rainbow trout fed the experimental diets under normoxic and hypoxic conditions.
Chronic hypoxia significantly increased plasma cortisol concentrations (+33%, Fig. 1) and moderately elevated plasma glucose levels (+4.3%), while inducing a shift towards a more oxidized hepatic redox status, as reflected by increased GSSG levels and a reduced GSH/GSSG ratio. Hypoxia also upregulated the expression of several antioxidant-related genes, including sod1, cat, gr and gclc, indicating activation of compensatory antioxidant mechanisms. Dietary krill meal supplementation attenuated the cortisol response under hypoxia, while plasma total antioxidant capacity remained consistently 6–10% higher in KM-fed fish than in CTRL fish, irrespective of oxygenation conditions (Fig. 1). Similar responses were observed for both Q1 and Q2 antioxidant fractions. Dietary treatment also modulated hepatic redox regulation, with significant effects on GSSG content, GSH/GSSG ratio and expression of genes involved in glutathione metabolism. In particular, expression of gr was enhanced in fish fed the highest krill meal level, supporting a role of KM in maintaining redox homeostasis. Interestingly, expression of the hypoxia-responsive marker egln3a remained unchanged after 3 weeks of hypoxia, possibly reflecting physiological acclimation to the moderate hypoxic challenge and a transient activation of canonical hypoxia-signalling pathways. Together, these findings indicate that krill meal supplementation enhances systemic antioxidant capacity while modulating hepatic redox regulation, thereby contributing to improved physiological adaptation to chronic hypoxic stress.
Conclusion
These findings demonstrate that dietary krill meal supplementation modulates both physiological stress and redox responses in rainbow trout exposed to chronic hypoxia. By attenuating cortisol response, enhancing systemic antioxidant capacity and influencing hepatic redox regulation, krill meal appears to support physiological robustness under environmental stress conditions. These results highlight the potential of krill meal as a functional ingredient to improve resilience of farmed salmonids facing increasingly variable oxygen conditions.
Acknowledgment
This work was supported by the EU H2020 Research Innovation Program (AQUAEXCEL3.0, PID30017).
References
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