Data from: Prior reproduction alters how mitochondria respond to an oxidative event
Data files
May 30, 2019 version files 113.65 KB
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Code for Hood et al 2019 X-ray Repro Study_revised March 29 2019.R
37.63 KB
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Final Data Summary_g March 29.csv
13.96 KB
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GLS Model Estimates March 29.csv
5.95 KB
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GLS Pup Model Results March 29.csv
5.44 KB
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Linear Model Estimates March 29.csv
5.95 KB
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Repro only dat March 29.csv
18.81 KB
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start.dat 3-29-19.csv
20.74 KB
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summary repro dat March 29.csv
5.16 KB
May 30, 2019 version files 113.65 KB
-
Code for Hood et al 2019 X-ray Repro Study_revised March 29 2019.R
37.63 KB
-
Final Data Summary_g March 29.csv
13.96 KB
-
GLS Model Estimates March 29.csv
5.95 KB
-
GLS Pup Model Results March 29.csv
5.44 KB
-
Linear Model Estimates March 29.csv
5.95 KB
-
Repro only dat March 29.csv
18.81 KB
-
start.dat 3-29-19.csv
20.74 KB
-
summary repro dat March 29.csv
5.16 KB
Abstract
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 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 female wild-derived house mice. Specifically, we compared mice that reproduced or were virgins to mice that were exposed to an oxidant (i.e., radiation) or not-exposed to radiation. 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 with 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.