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Sex Differences in Placental Mitochondrial Function Associated with Ozone-Induced Fetal Growth Restriction.
Citation:
Miller, C., K. Lavrich, D. Freeborn, J. Dye, P. Kodavanti, AND U. Kodavanti. Sex Differences in Placental Mitochondrial Function Associated with Ozone-Induced Fetal Growth Restriction. GEMS Fall Meeting, Durham, NC, November 09, 2016.
Impact/Purpose:
The purpose of this research is to provide evidence to support the emerging importance of mitochondrial function in the etiology of fetal growth restriction.
Description:
Fetal growth restriction is a major underlying cause of infant mortality worldwide. Unfortunately little is known about the mechanisms that drive compromised growth and the role of placental maladaptation on fetal development. In the current study placentas from male and female rat pups were harvested on gestational day (GD) 21 from Long Evans dams exposed to filtered air or 0.8 ppm ozone, 4hr/day during the implantation period on GD 5 and 6. At GD21, pups from ozone exposed dams had reduced weight compared to air control pups. Bioenergetics, measured as oxygen consumption rate (OCR), on mitochondria were measured using the Seahorse XF96 analyzer. Baseline OCR in the female placentas were elevated compared to males. While maternal ozone exposure did not impact female placental OCR at baseline, placentas of ozone-exposed males had increased OCR relative to controls. Following stimulation of the electron transport chain with ADP, a near significant effect of ozone to increase OCR was observed. Gene expression experiments confirmed elevated mitochondrial biogenesis in ozone-exposed male and female placentas. Further, female placentas from ozone-exposed dams had reduced Sod1 and increased Bcl2 expression compared to air-exposed female placentas. This difference was not observed in males. Together our data supports the hypothesis that placental mitochondrial dysfunction is related to reduced fetal weight. We demonstrate clear sex differences in the placental mitochondria of both healthy and growth compromised pups. Our findings support the emerging importance of mitochondrial function in the etiology of fetal growth restriction. This abstract does not reflect US EPA policy.