Abstract: Predator presence and shortage of food resources can alter behavior and cause chronic physiological stress, with long-term detrimental effects on the prey. Recently, it has been hypothesized that cellular damage via oxidative stress could be associated with such effects. Variation in food availability and predation risk could modify the oxidative/antioxidant status of prey. However, data from wild populations is scarce and, importantly, the interactive effects of these major ecological factors on oxidative/antioxidant status are poorly understood. We present the first study in a wild vertebrate, addressing the combined effects of experimental food supplementation and increased predation risk (cues of Mustela erminea) on antioxidant status of female pied flycatchers (Ficedula hypoleuca). We tested the effects during breeding, assuming that such variation could modify the antioxidant cost of reproduction. Supplementary food increased female body mass, independently of predator treatment. However, timing of breeding and reproductive investment remained unaffected by the treatments. Principal component 1 (PC 1) of antioxidant levels [reflecting superoxidase dismutase (SOD), glutathione peroxidase (GPx), and glutathione (tGSH)] showed lower values in the food-supplemented than non-food-supplemented group. Neither PC 2 [reflecting catalase (CAT) and GSH/GSSG ratio] nor PC 1 was affected by predation risk, and further, predation risk did not alter the effect of supplementary food on either PC. These results suggest that food resources may have a stronger impact than predation risk on female antioxidant status during breeding. This is the first fully experimental study focusing on the interactive effects of key environmental variables on antioxidant status in wild vertebrates; more studies are however needed to understand the role of these factors in shaping the cost of reproduction. Significance statement: Predator presence and shortage of food resources may modify animal behavior and cause chronic physiological stress response with long-term detrimental effects on the prey. Recently, it has been hypothesized that cellular damage via oxidative stress (i.e., imbalance between pro-oxidants and antioxidant defenses) could be associated with such effects, but evidence from wild populations is scarce. Importantly, the interactive effects of food and predation are not well understood. For the first time in a vertebrate, we experimentally studied the combined effects of food availability and (simulated) predation risk on antioxidant status, using wild breeding passerines. Higher food availability, but not increased perceived predation risk, lowered the antioxidant defenses. Predation risk did not alter the effect of supplementary food. The role of such interactions in shaping the cost of reproduction (via antioxidant/oxidative status) should be further studied.

Food supplementation, but not predation risk, alters female antioxidant status during breeding

Morosinotto C.;
2017

Abstract

Abstract: Predator presence and shortage of food resources can alter behavior and cause chronic physiological stress, with long-term detrimental effects on the prey. Recently, it has been hypothesized that cellular damage via oxidative stress could be associated with such effects. Variation in food availability and predation risk could modify the oxidative/antioxidant status of prey. However, data from wild populations is scarce and, importantly, the interactive effects of these major ecological factors on oxidative/antioxidant status are poorly understood. We present the first study in a wild vertebrate, addressing the combined effects of experimental food supplementation and increased predation risk (cues of Mustela erminea) on antioxidant status of female pied flycatchers (Ficedula hypoleuca). We tested the effects during breeding, assuming that such variation could modify the antioxidant cost of reproduction. Supplementary food increased female body mass, independently of predator treatment. However, timing of breeding and reproductive investment remained unaffected by the treatments. Principal component 1 (PC 1) of antioxidant levels [reflecting superoxidase dismutase (SOD), glutathione peroxidase (GPx), and glutathione (tGSH)] showed lower values in the food-supplemented than non-food-supplemented group. Neither PC 2 [reflecting catalase (CAT) and GSH/GSSG ratio] nor PC 1 was affected by predation risk, and further, predation risk did not alter the effect of supplementary food on either PC. These results suggest that food resources may have a stronger impact than predation risk on female antioxidant status during breeding. This is the first fully experimental study focusing on the interactive effects of key environmental variables on antioxidant status in wild vertebrates; more studies are however needed to understand the role of these factors in shaping the cost of reproduction. Significance statement: Predator presence and shortage of food resources may modify animal behavior and cause chronic physiological stress response with long-term detrimental effects on the prey. Recently, it has been hypothesized that cellular damage via oxidative stress (i.e., imbalance between pro-oxidants and antioxidant defenses) could be associated with such effects, but evidence from wild populations is scarce. Importantly, the interactive effects of food and predation are not well understood. For the first time in a vertebrate, we experimentally studied the combined effects of food availability and (simulated) predation risk on antioxidant status, using wild breeding passerines. Higher food availability, but not increased perceived predation risk, lowered the antioxidant defenses. Predation risk did not alter the effect of supplementary food. The role of such interactions in shaping the cost of reproduction (via antioxidant/oxidative status) should be further studied.
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/3497752
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 10
  • ???jsp.display-item.citation.isi??? 9
social impact