Chonnam Med J.
2006 Aug;42(2):101-107.
Changes in Protein Oxidation by Moxalactam in the Maternal Venous Plasma of Preterm Premature Rupture of Membranes
- Affiliations
-
- 1Department of Obstetrics and Gynecology, Chonnam National University Medical School, Chonnam National University Research Institute of Medical Sciences, Gwangju, Korea. kimyh@chonnam.ac.kr
- 2Department of Biochemistry, Chonnam National University Medical School, Chonnam National University Research Institute of Medical Sciences, Gwangju, Korea.
Abstract
- This study was performed to investigate the lipid peroxide levels and the basal, moxalactam, amoxacillin, and erythromycin-induced protein carbonyl contents in the maternal venous plasma of preterm premature rupture of membranes (PPROM) and normal pregnancy, and also to evaluate their roles in the pathophysiology of PPROM. Lipid peroxide level in the maternal venous plasma of each group was measured by thiobarbituric acid reaction. The protein carbonyl contents in that was determined by the 2, 4-dinitrophenylhydrazine (DNPH) method. Lipid peroxide levels in the maternal venous plasma of PPROM was significantly higher than that of normal pregnancy (5.73+/-0.48 vs. 3.45+/-0.25 nmol/mg protein, p<0.01). The basal protein carbonyl levels in the maternal venous plasma of PPROM was also significantly higher than that of normal pregnancy (7.81+/-0.39 vs. 6.85+/-0.25 nmol/mg protein, p<0.05). Protein carbonyl formation by moxalactam in the maternal venous plasma of PPROM was significantly higher than that of normal pregnancy (11.98+/-0.48 vs. 10.24+/-0.21 nmol/mg protein, p<0.01), but protein carbonyl formation by amoxacillin and erythromycin in the maternal venous plasma of PPROM was not significantly different from that of normal pregnancy. There was significant positive correlation between lipid peroxide levels and moxalactam-induced protein carbonyl levels of the maternal venous plasma (n=48, r=0.47, p<0.01). In summary, there was increased oxidative damage in the plasma lipid and protein of PPROM, and the oxidative damage, that is protein carbonyl formation, was aggravated by the moxalactam treatment. These results suggest that oxidative stress might be implicated to the onset of PPROM and the treatment with moxalactam would aggravate the disease by potentiating oxidative damage of the membrane protein.
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