Predation risk induces stress proteins and reduces antioxidant defense
Article first published online: 6 JUN 2008
© 2008 The Authors. Journal compilation © 2008 British Ecological Society
Volume 22, Issue 4, pages 637–642, August 2008
How to Cite
Slos, S. and Stoks, R. (2008), Predation risk induces stress proteins and reduces antioxidant defense. Functional Ecology, 22: 637–642. doi: 10.1111/j.1365-2435.2008.01424.x
- Issue published online: 11 JUL 2008
- Article first published online: 6 JUN 2008
- Received 31 January 2008; accepted 10 April 2008; Handling Editor: Peeter Hõrak
- damselfly larvae;
- fight-or-flight response;
- growth vs. mortality by predation trade-off;
- oxidative stress
- 1Despite its wide ecological relevance, we know little about the physiological mechanisms underlying the growth vs. mortality by predation trade-off. Here, we test for two costly, potential physiological correlates of the fight-or-flight response that may contribute to the growth reduction under predation risk: induction of stress proteins (Hsp60 and Hsp70) and of antioxidant enzymes (superoxide dismutase, SOD and catalase, CAT), in larvae of the damselfly Enallagma cyathigerum.
- 2Under predation risk, there was a growth reduction and an increase in oxygen consumption, indicative of the fight-or-flight response. Predation risk did not affect Hsp60 levels but induced an increase in energetically costly Hsp70 levels.
- 3Under predation risk, levels of SOD remained constant and those of CAT decreased. Together with the increase in respiration, this should inevitably result in oxidative stress.
- 4Our results suggest that induction of stress proteins may contribute to the partly physiologically mediated growth reduction under predation risk and that oxidative stress is a novel cost of predation risk that may have important long-term negative fitness consequences for the prey. The latter adds to the recent insight that costs of stressors and life-history trade-offs may not always directly operate through increased energy consumption and differential allocation, but, may also work through the increased production of reactive oxygen species.