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Short-term and long-term effects of transient exogenous cortisol manipulation on oxidative stress in juvenile brown trout
Author(s) -
Kim BirnieGauvin,
Kathryn S. Peiman,
Martin H. Larsen,
Kim Aarestrup,
William G. Willmore,
Steven J. Cooke
Publication year - 2017
Publication title -
journal of experimental biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.367
H-Index - 185
eISSN - 1477-9145
pISSN - 0022-0949
DOI - 10.1242/jeb.155465
Subject(s) - term (time) , juvenile , oxidative stress , trout , transient (computer programming) , brown trout , rainbow trout , biology , endocrinology , medicine , zoology , fishery , ecology , fish <actinopterygii> , physics , computer science , quantum mechanics , operating system
In the wild, animals are exposed to a growing number of stressors with increasing frequency and intensity, as a result of human activities and human-induced environmental change. To fully understand how wild organisms are affected by stressors, it is crucial to understand the physiology that underlies an organism's response to a stressor. Prolonged levels of elevated glucocorticoids are associated with a state of chronic stress and decreased fitness. Exogenous glucocorticoid manipulation reduces an individual's ability to forage, avoid predators and grow, thereby limiting the resources available for physiological functions like defence against oxidative stress. Using brown trout ( Salmo trutta ), we evaluated the short-term (2 weeks) and long-term (4 months over winter) effects of exogenous cortisol manipulations (versus relevant shams and controls) on the oxidative status of wild juveniles. Cortisol caused an increase in glutathione over a 2 week period and appeared to reduce glutathione over winter. Cortisol treatment did not affect oxidative stress levels or low molecular weight antioxidants. Cortisol caused a significant decrease in growth rates but did not affect predation risk. Over-winter survival in the stream was associated with low levels of oxidative stress and glutathione. Thus, oxidative stress may be a mechanism by which elevated cortisol causes negative physiological effects.

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