Background: Activation products from neutrophils and the complement system might cause endothelial dysfunction, which is central to the aetiology of pre-eclampsia. This study aimed to investigate the activity of myeloperoxidase (MPO), and its association with advanced oxidation protein products (AOPP), in women with pre-eclampsia and eclampsia.

Materials And Method: Twenty-one pregnant women with pre-eclampsia, 11 pregnant women with eclampsia and 19 healthy pregnant women were studied. Serum levels of malondialdehyde (MDA), AOPP, ascorbic acid (AA) and activities of MPO and catalase (CAT) were measured using a colorimetric method.

Results: The MDA level was significantly higher in the pre-eclampsia (3.15+/-0.28 nmol/mL) and eclampsia (4.01+/-0.66 nmol/mL) groups than in controls (1.85+/-0.18 nmol/mL); the difference between MDA levels in the pre-eclampsia and eclampsia groups was not statistically significant. MPO activity was significantly higher in the eclampsia (347.59+/-88.06 U/L) group than in the pre-eclampsia (196.17+/-30.8) and control (93.22+/-9.52) groups, and there was also no significant difference in these levels between the pre-eclampsia and control groups. CAT activity was significantly higher in the pre-eclampsia (166.35+/-31.75 U/L) and eclampsia (166.98+/-40.31 U/L) groups than in controls (81.28+/-7.41 U/L), and AA level was significantly higher in the pre-eclampsia (0.54+/-0.15 mg/dL) group than in controls (0.18+/-0.01 mg/dL); the differences in AA and CAT activity between the pre-eclampsia and eclampsia groups were not statistically significant. AOPP levels did not change significantly among the control, pre-eclampsia and eclampsia groups (106.88+/-5.62, 98.89+/-6.47, 111.89+/-6.8 micromol/L, respectively).

Conclusions: We suggest that increased oxidative stress might contribute to the pathophysiological mechanisms of pre-eclampsia and eclampsia, and that AA and CAT might have a protective role via free radical-scavenging properties. However, further study is needed.

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http://dx.doi.org/10.1111/j.1479-828X.2006.00647.xDOI Listing

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