title: Reproduction Does Not Adversely Affect Liver Mitochondrial Respiratory Function but Results in Lipid Peroxidation and Increased Antioxidants in House Mice.
abstract: Reproduction is thought to come at a cost to longevity. Based on the assumption that increased energy expenditure during reproduction is associated with increased free-radical production by mitochondria, oxidative damage has been suggested to drive this trade-off. We examined the impact of reproduction on liver mitochondrial function by utilizing post-reproductive and non-reproductive house mice (Mus musculus) living under semi-natural conditions. The age-matched post-reproductive and non-reproductive groups were compared after the reproductive females returned to a non-reproductive state, so that both groups were in the same physiological state at the time the liver was collected. Despite increased oxidative damage (p = 0.05) and elevated CuZnSOD (p = 0.002) and catalase (p = 0.04) protein levels, reproduction had no negative impacts on the respiratory function of liver mitochondria. Specifically, in a post-reproductive, maintenance state the mitochondrial coupling (i.e., respiratory control ratio) of mouse livers show no negative impacts of reproduction. In fact, there was a trend (p = 0.059) to suggest increased maximal oxygen consumption by liver mitochondria during the ADP stimulated state (i.e., state 3) in post-reproduction. These findings suggest that oxidative damage may not impair mitochondrial respiratory function and question the role of mitochondria in the trade-off between reproduction and longevity. In addition, the findings highlight the importance of quantifying the respiratory function of mitochondria in addition to measuring oxidative damage.
authors.affiliation: Department of Biological Sciences, Auburn University, Auburn, Alabama, United States of America.
authors.forename: Annelise V
authors.initials: AV
authors.lastname: Mowry
authors.affiliation: School of Kinesiology, Auburn University, Auburn, Alabama, United States of America.
authors.forename: Andreas N
authors.initials: AN
authors.lastname: Kavazis
authors.affiliation: Department of Biological Sciences, Auburn University, Auburn, Alabama, United States of America.
authors.forename: Aubrey E
authors.initials: AE
authors.lastname: Sirman
authors.affiliation: Department of Biology, University of Utah, Salt Lake City, Utah, United States of America.
authors.forename: Wayne K
authors.initials: WK
authors.lastname: Potts
authors.affiliation: Department of Biological Sciences, Auburn University, Auburn, Alabama, United States of America.
authors.forename: Wendy R
authors.initials: WR
authors.lastname: Hood
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D005260:Female; D015227:Lipid Peroxidation; D008136:Longevity; D008297:Male; D051379:Mice; D008930:Mitochondria, Liver / Q000378:metabolism*; D010085:Oxidative Phosphorylation; D018384:Oxidative Stress; D012098:Reproduction; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D002374:Catalase; D013482:Superoxide Dismutase