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Type of publication: Journal Article
Type of document: Full Paper

Year: 2004

Authors: Wiktor, H; Kankofer, M; Schmerold, I; Dadak, A; Lopucki, M; Niederm├╝ller, H

Title: Oxidative DNA damage in placentas from normal and pre-eclamptic pregnancies.

Source: Virchows Arch. 2004; 445(1):74-78

Authors Vetmeduni Vienna:

Dadak Agnes
Niederm├╝ller Hans
Schmerold Ivo

Vetmed Research Units
Institute of Pharmacology and Toxicology
Institute of Physiology, Pathohysiology and Biophysics, Unit of Physiology, Pathophysiology, and Experimental Endocrinology

Project(s): Investigations to determine oxidative damages of cellular DNA in animal and human organs

Placental oxidative stress was suggested to play a role in the pathogenesis of pre-eclampsia (PE). In this study, levels of 8-hydroxy-2"-deoxyguanosine (8-OH-dG), a well-established marker of oxidative DNA damage, were analysed in placental cellular DNA from normal (group NP) and pre-eclamptic (group PE) pregnancies as well as from PE pregnancies complicated by intrauterine growth restriction (group PE-IUGR). Placental samples obtained immediately after delivery were frozen at -80 degrees C until analysis. Cellular DNA was isolated, hydrolysed and analysed using high-performance liquid chromatography. Native nucleosides were monitored at 254 nm and 8-OH-dG using electrochemical detection. Concentrations of 8-OH-dG were expressed as micro mol/mol 2"-deoxyguanosine. In group NP, mean concentration of 8-OH-dG reached 179.97+/-80.58 (+/-SEM; micro mol/mol dG). 8-OH-dG levels were higher in group PE (273.44+/-110.14 micro mol/mol), but the difference was not significant in comparison with group NP. Highest concentrations of 8-OH-dG were found in group PE-IUGR (428.97+/-141.40 micro mol/mol), with levels significantly higher than in group NP, but not group PE. The results indicate a positive correlation between the severity of PE and the degree of oxidative stress and corroborate previous studies suggesting reactive oxygen species to be involved in the pathophysiology of PE.

Keywords Pubmed: DNA Damage*
Deoxyguanosine/analogs & derivatives*
Fetal Growth Retardation/etiology
Fetal Growth Retardation/metabolism
Fetal Growth Retardation/pathology
Infant, Newborn
Oxidative Stress*

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