• Journal of Environmental Health Sciences
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• v.46 no.4
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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 Applied Biological Chemistry
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• v.50 no.4
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• pp.249-253
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• 2007

Thirteen edible plants previously reported to show inhibitory activities on farnesyl protein transferase (FPTase) and phosphatase of the regenerating liver-3 (PRL-3) were evaluated for inhibitory activity on the proliferation of human umbilical vein endothelial cells (HUVECs). Four plant extracts, Oenothera erythrosepala, Perilla frutescens, Panicum miliaceum, and Quercus acutissima, significantly inhibited the proliferation of HUVECs induced by the basic fibroblast growth factor (bFGF) without cytotoxicity at 100 ${\mu}g/mL$. Myristica fragrans, Rosmarinus officinalis, and Syringa patula also showed inhibitory activity on the proliferation with only mild cytotoxicity.

• Asian-Australasian Journal of Animal Sciences
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• v.20 no.9
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• pp.1342-1348
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• 2007

POU1F1 is a positive regulator for GH, PRL and TSH${\beta}$ and its mutations associate with production traits in ruminant animals. We described a DdeI PCR-RFLP method for detecting a silent allele in the goat POU1F1 gene: TCT (241Ser)>TCG (241Ser). Frequencies of $D_1$ allele varied from 0.600 to 1.000 in Chinese 801 goats. Significant associations of DdeI polymorphism with production traits were found in milk yield (*p<0.05), litter size (*p<0.05) and one-year-old weight (*p<0.05) between different genotypes. Individuals with genotype $D_1D_1$ had a superior performances when compared to those with genotype $D_1D_2$ (*p<0.05). Hence, the POU1F1 gene was suggested to the potential candidate gene for superior milk performance, reproduction trait and weight trait. Genotype $D_1D_1$, characterized by a DdeI PCR-RFLP detection, was recommended to geneticists and breeders as a molecular marker for better performance in the goat industry.