Meeting Abstract
A central tenet of biology is that the costs of reproduction contribute to earlier senescence. Because reproduction is energetically demanding, it has been assumed that reproduction stimulates the production of reactive oxygen species that damage cells and hasten aging. Yet, several studies have shown that oxidative damage is typically unchanged or reduced in reproductive individuals when compared to non-reproductive controls. To evaluate the relative cost of reproduction, we quantified mitochondrial function in the liver of house mice that bred several times verses those that never bred. Mice were maintained in enclosures that mimic the conditions of free-living wild mice. Reproductive females had the opportunity to breed for 8 months, while non-reproductive females were maintained for a similar duration with infertile male(s). At 10.5 months, the males were removed to curtail breeding. Females were sacrificed at 12 months of age and liver mitochondria were isolated by differential centrifugation and used for analyses. The respiratory control ratio (RCR) of reproductive females was not different compared to non-reproductive females (p=0.16). Oxidative damage of liver mitochondria, as measured by 4 hydroxynonenal (4HNE), trended to be higher in reproductive mice (p=0.09), despite having higher mitochondrial protein levels of antioxidants (i.e., SOD2 and catalase) (p<0.05). Thus, our data indicate that enhanced antioxidant protein production may have been insufficient to prevent oxidative damage to liver mitochondria in animals that reproduced for 8 months. However, additional studies are needed to fully elucidate how mitochondrial function changes with parity and differs among metabolically active tissues.
