The proximal costs of case construction in caddisflies: antioxidant and life history responses

Abstract

SUMMARYAnimal construction allows organisms to cope with environmental variations but the physiological costs of such behaviour are still poorly understood. The aim of the present study was to measure the physiological cost of construction behaviour through the oxidative balance that is known to affect the ability of organs to function, stimulates senescence processes and ultimately impacts the fitness of the organism. We used larvae of caddisfly, Limnephilus rhombicus, by experimentally modifying the effort associated with case building. Larvae that were forced to build a new case showed a significant increase in both total antioxidant capacity and the specific activity of superoxide dismutase 48 and 72h, respectively, after the initiation of the reconstruction. These results strongly suggest that the larval construction behaviour triggered the production of reactive oxygen species, but their effects were reversed 7days after the reconstruction. In the animals that were forced to build a new case, oxidative stress appeared to be mitigated by a network of antioxidant defences because no oxidative damage was observed in proteins compared with the control larvae. At the adult stage, while longevity was not sex dependent and was not affected by the treatment, body mass and body size of adult males from the reconstruction treatment were significantly lower than the control values. This unexpected sex effect together with data on oxidative stress highlights the difficulty of determining the physiological cost associated with energy-demanding behaviours, implying a consideration of both their energetic and non-energetic components is required.

Detrital nutrient content determines growth rate and elemental composition of bromeliad‐dwelling insects

“…It is also possible that caddisflies have behavioural and physiological mechanisms to store P in their bodies while they are growing (see Frost & Elser, for mayfly responses to P enrichment). Since most caddisfly adults do not feed, the larva is the only stage of resource acquisition (Mondy et al ., ). Overall, our results show that growth rate responses of chironomids and caddisflies to P and N may reflect physiological as well as ecological differences in the identity of the growth‐limiting nutrient.…”

“…At present, it is not clear why the growth of caddisflies is limited more by N than by P, but we note that caddisflies have replaced a chitinous exoskeleton with a protective case built from leaf material scavenged in their environment, glued together with adhesive silk (Stewart & Wang, ). This silk is composed primarily of proteins and thus is a compound rich in N (Ohkawa et al ., ), imposing high N requirements for caddisflies (Mondy, Rey & Voituron, ). A possible explanation for the higher body P content with growth in caddisflies, but lack of P‐limited growth is that caddisflies may have high P assimilation (and higher than chironomids) (see He & Wang, ).…”

Plasma markers of oxidative stress are uncorrelated in a wild mammal

“…A growing number of studies provide evidence for associations among markers of OS and life-history traits (Salmon et al 2001;Alonso-Alvarez et al 2007;Catoni et al 2008;Nussey et al 2009;Archer et al 2012;Mondy et al 2012;Rubolini et al 2012). However, an important question still remains: Can we draw general conclusions about patterns of variation in OS and their consequences for life histories from just one or a few markers, or Are the findings of any one study of OS likely to be specific to the markers selected and the context in which they are measured?…”

Mechanistic, ecological, and evolutionary consequences of artificial light at night for insects: review and prospective

“…This hormone protects lipid, protein, and DNA molecules against damage caused by free radicals by acting as a direct scavenger to detoxify reactive oxygen and nitrogen species (Reiter et al., ). Reactive oxygen species (ROS) are mainly produced by mitochondria (oxidative phosphorylation) during ATP production (e.g., Monaghan et al., ; Mondy et al., ). Although low levels of ROS play a role in cell signaling and induction of defense genes, an excessive release of ROS induces oxidative stress that leads to loss of cell functions and programmed cell death.…”