![]() ![]() The ability to mount an adequate stress response dictates whether an organism survives and thrives during physiological challenges (Parsons 2005 Blas et al. Fitness consequences of stress may thus be accentuated during periods of rapid environmental change. These data support the life-history-oxidative stress hypothesis in a capital breeding mammal and suggest lactation is a period of heightened vulnerability to environmental factors that exacerbate cellular stress. Cellular stress, and the ability to mount effective cellular defences, could proscribe lactation strategy in grey seal mothers and thus affect pup survival probability. Higher glutathione peroxidase ( GPx) and lower catalase ( CAT) were associated with longer lactation but reduced maternal transfer efficiency and lower pup weaning mass. Pups whose mothers had higher blubber glutathione-S-transferase ( GST) expression at early lactation gained mass more slowly. Lactation duration and maternal mass loss rate were both positively related to pup weaning mass. Foraging females had higher mRNA abundance of some Hsps and lower RE transcript abundance and MDA concentrations, suggesting they experienced lower oxidative stress than lactating mothers, which diverted resources into pup rearing at the expense of blubber tissue damage. ![]() ![]() Transcript abundance of Hsc70 increased, and Nox4, a pro-oxidant enzyme, decreased throughout lactation. We investigated oxidative damage (malondialdehyde (MDA) concentration) and cellular defences (relative mRNA abundance of heat shock proteins ( Hsps) and redox enzymes ( REs)) in blubber of wild female grey seals during the lactation fast ( nā=ā17) and summer foraging ( nā=ā13). As capital breeders, grey seals are a natural system in which to test this theory. Life-history-oxidative stress theory predicts that elevated energy costs during reproduction reduce allocation to defences and increase cellular stress, with fitness consequences, particularly when resources are limited. ![]()
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