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Original Article
- Placental Superoxide Dismutase, Genetic Polymorphism, and Neonatal Birth Weight.
- Yun Chul Hong, Kwan Hee Lee, Moon Whan Im, Young Ju Kim, Eun Hee Ha
- J Prev Med Public Health. 2004;37(4):306-311. Published online November 30, 2004
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Abstract
PDF - BACKGROUND
The roles of antioxidants in the placenta and genetic susceptibility to oxidant chemicals in relation to neonatal birth weight have not been elucidated. We determined whether the level of placental manganese superoxide dismutase (MnSOD) and its genetic polymorphism plays any role in oxidative stress and neonatal birth weight. METHODS: We measured placental MnSOD and determined MnSOD genetic polymorphism among 108 pregnant women who were hospitalized for delivery and their singleton live births in Korea. Main outcome measurements are maternal urinary malondialdehyde (MDA) and birth weight. RESULTS: Maternal urinary concentrations of MDA were significantly associated with neonatal birth weight (P=0.04). The enzyme level of placental MnSOD was also significantly associated with MDA concentration (P=0.04) and neonatal birth weight (P< 0.01). We observed dose-response relationships between placental MnSOD and maternal urinary MDA, and neonatal birth weight after adjusting for maternal weight, height, age, and neonatal sex. After controlling for covariates, MnSOD variant genotype increased maternal urinary MDA concentrations (P< 0.01) and reduced birth weight by 149 gm (P=0.08). CONCLUSIONS: This study demonstrates that the placental level of MnSOD during pregnancy significantly affects fetal growth by reducing oxidative stress, and that genetic polymorphism of MnSOD probably modulate the effects of oxidants on fetal growth. -
SummaryEnglish Abstracts
- Folate and Homocysteine Levels during Pregnancy affect DNA Methylation in Human Placenta.
- Bo hyun Park, Young Ju Kim, Jong soon Park, Hwa young Lee, Eun hee Ha, Jung won Min, Hye sook Park
- J Prev Med Public Health. 2005;38(4):437-442.
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Abstract
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- OBJECTIVES
DNA methylation is one of the best characterized epigenetic mechanisms that play a regulatory role in genome programming and imprinting during embryogenesis. In this present study, we investigated the association between DNA methylation in the human placenta and the maternal folate and homocysteine concentrations on the Methylenetetrahydrofolatereductase (MTHFR) genetic polymorphism during pregnancy. METHODS: We investigated 107 pregnant women who visited Ewha Woman's University Hospital for prenatal care during their 24~28 weeks-period of gestation. During the second trimester, we measured the serum homocysteine and folate concentrations. The MTHFR 677 genetic polymorphism was determine by performing PCR-RFLP assay. The expression of DNA methylation in the human placentas was estimated by using immunohistochemistry method. RESULTS: Serum folate was negatively correlated with the serum homocysteine concentration for all the MTHFR genotypes. We found positive correlation between the folate concentrations and the DNA methylation in the human placenta (p< 0.05). An increasing concentration of homocysteine was associated with reduced DNA methylation in the human placenta. The coefficient value was -2.03 (-3.77, -0.29) on the regression model (p< 0.05). CONCLUSION: These findings suggest that the maternal folate and homocysteine levels along with the MTHFR 677 genetic polymorphism during pregnancy affect the DNA methylation in the human placenta. -
Summary
- Effects of Bisphenol A on the Placental Function and Reproduction in Rats.
- Chae Kwan Lee, Seog Hyun Kim, Deog Hwan Moon, Jeong Ho Kim, Byung Chul Son, Dae Hwan Kim, Chang Hee Lee, Hwi Dong Kim, Jung Won Kim, Jong Eun Kim, Chae Un Lee
- J Prev Med Public Health. 2005;38(3):330-336.
- 2,498 View
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Abstract
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- OBJECTIVE
The aim of this study was to investigate the effects of bisphenol A (BPA), an estrogen-like environmental endocrine disrupter, on the placental function and reproduction in rats. The mRNA levels of the placental prolactin-growth hormone (PRL-GH) gene family, placental trophoblast cell frequency and reproductive data were analyzed. METHODS: The pregnancies of F344 Fisher rats (160 g +/- 20 g) were detected by the presence of the copulatory plug or sperm in the vaginal smear, which marked Day 0 of pregnancy. Pregnant rats were divided into three groups. The control group was intraperitoneally injected with a sesame oil vehicle. The two remaining groups were injected with 50 or 500 mg/kg B.W/day of BPA, resuspended in sesame oil, on either days 7 to 11 or 16 to 20 of pregnancy, with the rats sacrificed on either day 11 or 20, respectively. The mRNA levels of PRL-GH and Pit-1a and b isotype genes were analyzed by Northern blot hybridization and reverse transcription-polymerase chain reaction. The hormone concentrations were analyzed by radioimmunoassay, and the frequency of the placental trophoblast cells observed by a histochemical study. Reproductive data, such as the placental weight and litter size, were surveyed on day 20. The fetal weight was surveyed for 4 weeks after birth. A statistical analysis was carried out using the SAS program (version 8.1). RESULTS: The mRNA levels of the PRL-GH gene family, such as placental lactogen I, Iv and II, prolactin like protein A, C and Cv, and decidual prolactin-related protein were significantly reduced due to BPA exposure. The mRNA levels of the Pit-1a and b isotype genes, which induce the expression of the PRL-GH gene family in the rat placenta, were also reduced due to BPA exposure. The PL-Iv and PL-II concentrations were reduced in the BPA exposed group. During the middle to last stage of pregnancy (Days 11-20), a high dose of BPA exposure reduced the frequency of spongiotrophoblast cells, which are responsible for the secretion of the PRL-GH hormones. Reproductive data, such as the placental and fetal weights and the litter size, were reduced, but that of the pregnancy period was extended in the BPA exposed compared to the control group. CONCLUSIONS: BPA disrupts the placental functions in rats, which leads to reproductive disorders. -
SummaryOriginal Article
- Effects of Chromium (VI) Exposure on the Placental Function and Reproduction in Rats.
- Heun Lee, Jin Ho Chun, Deog Hwan Moon, Chae Un Lee, Sung Goo Kang, Byung Chul Son, Dae Hwan Kim, Chang Hee Lee, Jung Won Kim, Chae Kwan Lee
- J Prev Med Public Health. 2004;37(2):157-165.
- 2,459 View
- 61 Download
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Abstract
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- OBJECTIONS: This study aimed to investigate the toxic effects of chromium (VI) on the placental function and reproduction in rats. For the study, the placental prolactin-growth hormone (PRL-GH) gene expression, placental trophoblast cell differentiation and reproductive data were analyzed. METHODS: The pregnancies of F344 Fisher rats were checked by the presence of a copulatory plug or sperm in the vaginal smear, which was defined as day 0 of the pregnancy. Pregnant rats were divided into the three groups. The control group was given tap water (chromium level < 0.001 ppm) and the remaining groups were given 250 or 750 ppm of chromium (VI) [as potassium dichromate], from day 7 to 19 of the pregnancy. Rats were sacrificed at days 11 and 20 of pregnancy. The mRNA levels of PRL-GH and Pit-1a and b isotype genes were analyzed by Northern blot hybridization and reverse transcriptionpolymerase chain reaction (RT-PCR). The hormonal concentration was analyzed by radioimmunoassay, and the differentiation of placental trophoblast cells were observed by histochemical studies. Reproductive data, such as placental and fetal weights, pregnancy period, and litter size, were surveyed at day 20 of pregnancy and after birth. A statistical analysis was carried out using the SAS program (version 8.1). RESULTS: The mRNA levels of the prolactin-growth hormone (PRL-GH) family of genes were dose dependently reduced by chromium exposure. The mRNA levels of Pit-1a and b isotype genes that induce the expression of the PRL-GH family of genes were also reduced by chromium exposure. The PRL-GH hormonal concentration in the rat placenta, fetus and maternal blood were decreased by chromium exposure. In the middle stage of pregnancy (day 11), a high dose of chromium suppressed the differentiation of spongiotrophoblast cells that secret the PRLGH hormones. In the last stage of pregnancy (day 20), a high dose of chromium induced apoptosis of placental cells. Reproductive data, such as placental and fetal weights, litter size, were reduced, but the pregnancy period was extended in the group exposed to chromium compared with the controls. CONCLUSION: Chromium (VI) disrupts the ordered functions of the placenta, which leads to reproductive disorders in rats.
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