PLACENTAL MITOCHONDRIAL-DNA AND RESPIRATORY-CHAIN ENZYMES IN THE ETIOLOGY OF PREECLAMPSIA

Citation
K. Vuorinen et al., PLACENTAL MITOCHONDRIAL-DNA AND RESPIRATORY-CHAIN ENZYMES IN THE ETIOLOGY OF PREECLAMPSIA, Obstetrics and gynecology, 91(6), 1998, pp. 950-955
Citations number
26
Categorie Soggetti
Obsetric & Gynecology
Journal title
ISSN journal
00297844
Volume
91
Issue
6
Year of publication
1998
Pages
950 - 955
Database
ISI
SICI code
0029-7844(1998)91:6<950:PMAREI>2.0.ZU;2-T
Abstract
Objective: To evaluate the occurrence of the most common mutations and deletions in mitochondrial DNA and deficiencies in the enzyme complex es of the mitochondrial respiratory chain in placentas from preeclampt ic 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 Souther n blot and polymerase chain reaction (PCR) methods from the same place ntas. Results: Mean (+/- standard deviation) mitochondrial respiratory chain enzyme complex activities in placentas on protein basis (nmol/m in/mg of protein) were similar in preeclamptics and controls (nicotina mide adenine dinucleotide, reduced form-ubiquinone oxidoreductase 25.8 4 +/- 9.29 versus 31.02 +/- 7.52; nicotinamide adenine dinucleotide, r educed form-cytochrome-e oxidoreductase 77.88 +/- 42.24 versus 104.06 +/- 56.73; succinate-cytochrome-c oxidoreductase 57.90 +/- 13.83 versu s 64.44 +/- 20.16; cytochrome-e oxidase 106.43 +/- 35.46 versus 128.37 +/- 48.64, respectively) and they were similar also when referenced t o the mitochondrial marker enzyme citrate synthase. The sample sizes i n both patient and control groups were found to be large enough by pos t hoc test. Large-scale deletions or the common 5-kb and 7.4-kb deleti ons were not detected, even at the sensitivity level of PCR. The three most common point mutations were not found in either control or preec lamptic placental samples. Conclusion: Common mitochondrial DNA mutati ons seem to play no major role in the universal etiology of preeclamps ia, as assessed by analysis of the mitochondrial genome and respirator y chain enzyme activities in vitro. This does not exclude possible alt erations in the energy state of the preeclamptic placenta. (C) 1998 by The American College of Obstetricians and Gynecologists.