Placental mitochondrial DNA and respiratory chain enzymes in the etiology of preeclampsia

OBJECTIVE: To evaluate the occurrence of the most common mutations and deletions in mitochondrial DNA and deficiencies in the enzyme complexes of the mitochondrial respiratory chain in placentas from preeclamptic women. METHODS: Mitochondria were isolated from the placentas of 17 preeclamptic or 25 control women, and the activities of mitochondrial respiratory chain complexes were measured. Deletions and three common point mutations of mitochondrial DNA were searched for by the Southern blot and polymerase chain reaction (PCR) methods from the same placentas. RESULTS: Mean (+/- standard deviation) mitochondrial respiratory chain enzyme complex activities in placentas on protein basis (nmol/min/mg of protein) were similar in preeclamptics and controls (nicotinamide adenine dinucleotide, reduced form-ubiquinone oxidoreductase 25.84 +/- 9.29 versus 31.02 +/- 7.52; nicotinamide adenine dinucleotide, reduced form-cytochrome-c oxidoreductase 77.88 +/- 42.24 versus 104.06 +/- 56.73; succinate-cytochrome-c oxidoreductase 57.90 +/- 13.83 versus 64.44 +/- 20.16; cytochrome-c oxidase 106.43 +/- 35.46 versus 128.37 +/- 48.64, respectively) and they were similar also when referenced to the mitochondrial marker enzyme citrate synthase. The sample sizes in both patient and control groups were found to be large enough by post hoc test. Large-scale deletions or the common 5-kb and 7.4-kb deletions were not detected, even at the sensitivity level of PCR. The three most common point mutations were not found in either control or preeclamptic placental samples. CONCLUSION: Common mitochondrial DNA mutations seem to play no major role in the universal etiology of preeclampsia, as assessed by analysis of the mitochondrial genome and respiratory chain enzyme activities in vitro. This does not exclude possible alterations in the energy state of the preeclamptic placenta.

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