As acute stress induced by predation risk can generate significant oxidative damage, prey organisms are forced to balance their defence reaction and the cost of activating the cellular defence system. Stress tolerance differs significantly among species; therefore predator pressure indirectly shapes the community structure. To test adaptation abilities of amphipod crustaceans (Dikerogammarus villosus and Gammarus jazdzewskii) we exposed them to acute (35 min.) and chronic (1 or 7 days) predation risk (the Eurasian perch). We measured respiration (related to metabolic rate), cellular defence systems (antioxidant enzyme (catalase) activity and heat shock protein (Hsp70) concentration), and the level of oxidative damage (thiobarbituric acid reactive substances (TBARS) concentration). Both amphipods increased their respiration rate in the presence of predation cues, irrespective of the duration of their pre-exposure to danger. This increase in D. villosus was initiated more quickly (immediately vs. after 10 min. of the test) and lasted for a longer time (20 vs. 10 min.) than in G. jazdzewskii. However, only G. jazdzewskii after a short exposure to predation risk exhibited an increase in its catalase activity, Hsp70 concentration and oxidative damage. No changes in these parameters were exhibited by D. villosus or after a chronic exposure of G. jazdzewskii to predation cues. Our results show that prey organisms are able to reconfigure their physiology to maintain increased metabolic rate under prolonged predator pressure and, at the same time, reduce oxidative damage as well as costs related to anti-oxidant defence.

During summer land snails are repeatedly exposed to low oxygen tension and to enhanced production of reactive oxygen species due to aestivation/arousal cycles. To test the role of reduced glutathione (GSH – the main endogenous antioxidant) and effect of season on its function we examined activities of glutathione-related enzymes and concentration of GSH in Helix pomatia snails (1) during their natural aestivation/arousal cycle in summer and (2) after their acclimation to different thermal and photoperiod conditions in autumn. Natural aestivation evoked decreases in activity of glutathione reductase (GR) in the hepatopancreas and kidney and an increase in activity of glutathione transferase (GST) in the hepatopancreas, but did not affect activity of glutathione peroxidase (GPX) and concentration of GSH in these organs. Activities of GR in both organs and GST in the kidney were highly affected by acclimation to summer-specific ambient conditions, whereas activity of GPX and GSH concentration were affected by acclimation to 25°C at a short-day photoperiod. In conclusion, H. pomatia maintains relatively high organ concentrations of reduced glutathione but can also modulate its enzymatic antioxidant defence system according to environmental conditions.

Hypoxic-ischaemic brain injury involves increased oxidative stress. In asphyxiated newborns iron deposited in the brain catalyses formation of reactive oxygen species. Glutathione (GSH) and vitamin E are key factors protecting cells against such agents. Our previous investigation has demonstrated that newborn rats, showing physiological low body temperature as well as their hyperthermic counterparts injected with deferoxamine (DF) are protected against iron-mediated, delayed neurotoxicity of perinatal asphyxia. Therefore, we decided to study the effects of body temperature and DF on the antioxidant status of the brain in rats exposed neonatally to critical anoxia. Two-day-old newborn rats were exposed to anoxia in 100% nitrogen atmosphere for 10 min. Rectal temperature was kept at 33 °C (physiological to rat neonates), or elevated to the level typical of healthy adult rats (37 °C), or of febrile adult rats (39 °C). Half of the rats exposed to anoxia under extremely hyperthermic conditions (39 °C) were injected with DF. Cerebral concentrations of malondialdehyde (MDA, lipid peroxidation marker) and the levels of GSH and vitamin E were determined post-mortem, (1) immediately after anoxia, (2) 3 days, (3) 7 days, and (4) 2 weeks after anoxia. There were no post-anoxic changes in MDA, GSH and vitamin E concentrations in newborn rats kept at body temperature of 33 °C. In contrast, perinatal anoxia at elevated body temperatures intensified oxidative stress and depleted the antioxidant pool in a temperature-dependent manner. Both the depletion of antioxidants and lipid peroxidation were prevented by post-anoxic DF injection. The data support the idea that hyperthermia may extend perinatal anoxia-induced brain lesions.