• 한국환경보건학회지
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• 제46권4호
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• pp.368-375
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• 2020

Objectives: Some animal studies have reported that methyl mercury causes developmental toxicities such as placental and fetal weight loss, but the mechanism is still unclear. This study aimed to investigate the developmental toxicities of methyl mercury, focusing on placental endocrine function and fetal growth retardation in rats. Methods: Positively same-time-mated female Sprague-Dawley rats were purchased on gestational day (GD) eight and treated with 0, 5, 10 and 20 ppm of methyl mercury (n=5) dissolved in tap water from GD eight through 19. During treatment, the drinking water (methyl mercury) intake and body weight of each pregnant rat was measured daily. On day 19, caesarean sections were performed and blood samples were collected. Developmental data such as placental and fetal weights, fetus numbers, and placental efficiency (fetal weight/placental weight) were also collected. Placental prolactin-growth hormone (PRL-GH) family, such as placental lactogen (PL) -Iv, II, and prolactin-like protein (PLP) -B, levels in serum were analyzed by ELISA. Also, placental tissues were assigned to histochemistry. Results: The mean cumulative methyl mercury exposure for the 5, 10, and 20 ppm groups were 2.37, 4.63, and 9.66 mg, respectively. The mean daily exposure of the 5, 10, and 20 ppm groups were 0.24, 0.47, and 0.97 mg, respectively. Maternal body weight increased in accordance with GD. There was no significant difference in weight gain among the experimental groups. Histopathologic changes were not observed in placental tissues among the experimental groups. However, mean placental and fetal weights were lower in the 10 and 20 ppm exposed groups compared to the control. Placental efficiency was also lower in the 10 and 20 ppm exposed groups compared to the control. Serum PL-Iv and II levels were lower in the 10 and 20 ppm exposed groups than the control, in accordance with the changing pattern of placental and fetal weights and placental efficiency. Conclusion: The inhibitory effects of methyl mercury on the serum levels of placental PRL-GH family such as PL-Iv and II may be secondary leads to the reduction of placental efficiency and fetal growth retardation in rats.

• Journal of Preventive Medicine and Public Health
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• 제37권2호
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• pp.157-165
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• 2004

Objectives : 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 transcription-polymerase 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.

• Journal of Preventive Medicine and Public Health
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• 제38권3호
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• pp.330-336
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• 2005

Objectives : 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 ($160g{\pm}20g$) 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.