Oxidative Stress Impairs Fatty Acid Oxidation and Mitochondrial Function in the Term Placenta

Placental fatty acid oxidation (FAO) is impaired and lipid storage is increased in pregnancy states associated with chronic oxidative stress. The effect of acute oxidative stress, as seen in pregnancies complicated with asthma, on placental lipid metabolism is unknown. We hypothesized that induction of acute oxidative stress would decrease FAO and increase esterification. We assessed [ 3 H]-palmitate oxidation and esterification in term placental explants from lean women after exposure to hydrogen peroxide (H 2 O 2 ) for 4 hours. Fatty acid oxidation decreased 16% and 24% in placental explants exposed to 200 ( P =.02) and 400 µM H 2 O 2 ( P =.01), respectively. Esterification was not altered with H 2 O 2 exposure. Neither messenger RNA nor protein expression of key genes involved in FAO (eg, peroxisome proliferator-activated receptor α, carnitine palmitoyl transferase 1b) were altered. Adenosine triphosphate (ATP) levels decreased with induction of oxidative stress, without increasing cytotoxicity. Acute oxidative stress decreased FAO and ATP production in the term placenta without altering fatty acid esterification. As decreases in placental FAO and ATP production are associated with impaired fetal growth, pregnancies exposed to acute oxidative stress may be at risk for fetal growth restriction.