Prior reproduction alters how mitochondria respond to an oxidative event.

An animal's pace of life is mediated by the physiological demands and stressors it experiences (e.g. reproduction) and one likely mechanism that underlies these effects is oxidative stress. Reproduction has been shown to increase or reduce oxidative stress under different conditions and to modify mitochondrial performance. We hypothesized that the changes associated with reproduction can alter how animals respond to future oxidative stressors. We tested this theory by comparing the organ-specific mitochondrial response in wild-derived female house mice. Specifically, we examined the effect of an oxidant (X-irradiation) on virgin mice and on mice that had reproduced. We measured liver and skeletal muscle mitochondrial density, respiratory performance, enzyme activity and oxidant production, as well as markers of oxidative damage to tissues. In the liver, prior reproduction prevented a radiation-induced reduction in mitochondrial density and increased mitochondrial respiratory performance. In skeletal muscle, prior reproduction resulted in a radiation-induced decline in mitochondrial density which could reduce the bioenergetic capacity of skeletal muscle mitochondria. Yet, electron transport chain complex I activity in skeletal muscle, which dropped after reproduction, returned to control levels following oxidant exposure. The results of this investigation indicate that prior reproduction alters the response of mitochondria to an oxidative challenge in an organ-specific manner. Such changes could have differential effects on future reproductive performance and risk of death.