• Proceedings of the Korean Aquaculture Society Conference
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• 2003.10a
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• pp.145-145
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• 2003

To evaluate the effect of PAHs on fertilization and larval development of the Pacific oyster, Crassostrea gigas via in vivo exposure for 30 days. Conditioned C. gigas adult brood stock was taken from oyster farm in May 2003 and raised in flow through tank at 20-22$^{\circ}C$ with feeding equivalently mixed marine microalgae: Chaetoceros simplex, C. gracilis, Isochrysis galbana and Tetrasemis tetrathele. The oysters were exposed to PAHs cocktail at 200ppb (10 species) until they are fully riped with an untreated group. Motility of sperm, Fertilization and The percent of D-shaped larvae was measured under microscope (Olympus BX-50). Fertilization capability using dry sperm and eggs from both non- and PAHs treated brood stocks was significantly reduced at the treated group (P<0.01). In addition to the origin effect, it was obvious that fertilization of eggs from both group were adversely suppressed in consistent with PAHs level (P<0.01). The percent of D-shaped larvae in treated group was significantly reduced comparing to non-treated. The percent was adversely correlated with PAHs level, which was more significantly reduced in treated group. Therefore, it was obvious that PAHs exposure on the Pacific oyster has adverse affects on the sperm as well as larvae in both maternal and acute source.

• BioChip Journal
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• v.12 no.4
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• pp.304-308
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• 2018

Atopic disease is caused by a complex combination of environmental factors and genetic factors, and studies on influence of exposure to various environmental factors on atopic diseases are continuously reported. However, the exact cause of atopic dermatitis is not yet known. Our study was conducted to analyse the association of SNPs with the development of atopic disease in a small cohort. Samples were collected from the Mothers' and Children's Environmental Health (MOCEH) study and 192 cord blood DNA samples were used to identify incidence of atopy due to influence of exposure to environmental factors. Genetic elements were analysed using a precision medicine research (PMR) array designed with various SNPs for personalized medicine. Case-control analysis of atopy disease revealed 253 significant variants (p<0.0001) and SNPs on five genes (CARD11, ZNF365, KIF3A, DMRTA1, and SFMBT1) were variants identified in previous atopic studies. These results are important to confirm the genetic mutation that may lead to the onset of foetal atopy due to maternal exposure to harmful environmental factors. Our results also suggest that a small-scale genome-wide association analysis is beneficial to confirm specific variants as direct factors in the development of atopy.

• Journal of Preventive Medicine and Public Health
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• v.22 no.1 s.25
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• pp.71-80
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• 1989

The adverse effect of diving on the fetus may extend beyond n gestational process and outcome. Primiparous Sprague-Dawley rats were assigned to one of ten exposure schedules during gestatred $PO_2$ level, the following question about the effect of exposing a pregnant female to high partial pressure of inspired oxygen has been raised. 'What effect does an increased maternal $PIO_2$ have on fetal arterial $PO_2$ and therefore on possible fetal oxygen poisoning?' This study was carried out to observe the effects of maternal hyperoxia on gestational process and outcome. Primiparous Sprague-Dawley rats were assigned to one of ten exposure schedules during gestation. The treatment groups were subjected to either the high concentration of oxygen, or the high atmospheric pressure. On day 21 of gestation, laparotomy was performed to examine for number and distribution of implantations and live and resorbing embryos. Fetuses were weighed, and examined for gross malformations. Subsequently, they were fixed, measured in physical parameters, and examined for visceral anomalies. Minor visceral anomalies and anatomical variation was not found. Similarily, there were no significant differences when number of resorptions, mean fetal weights, pregnancy interruption rate were compared by analysis of variance. These results indicate that exposing rats to oxygen at increased atmospheric pressure doese not affect fetal health or survival.

• Toxicological Research
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• v.25 no.4
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• pp.209-216
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• 2009

We have recently reported that the continuous exposure of rats to a concrete building environment under cool temperatures had adverse effects on general health parameters and embryo-fetal development. This study examined to compare the potential effects of concrete and wood building environments on pregnant dams and embryo-fetal development in rats. Groups of 10 mated females were exposed to polycarbonate (control), concrete, or wood cages from gestational days (GD) 0 to 20 under cool temperatures $(11.9\sim12.3^{\circ}C)$. All the females underwent a caesarean section on GD 20, and their fetuses were examined for any morphological abnormalities. The temperatures in the cages were similar in all groups but the relative humidity in the concrete and wood groups were higher than in the control group. The concentration of volatile organic compounds in the wood group was higher than in the control group. In the concrete group, maternal effects manifested as an increase in the incidence of clinical signs, a lower body weight, and a decrease in the thymus and ovary weights. Developmental effects included increased post-implantation loss and decreased litter size. Infrared thermal analysis showed that the skin temperature of the rats in the concrete group was lower than that in the control group. In contrast, there were no exposure-related adverse effects on the maternal and developmental parameters in the wood group. Overall, the exposure of pregnant rats to a concrete building environment under cool temperatures has adverse effects on the clinical signs, body weight, skin temperature, organ weight, and embryo-fetal development. On the other hand, exposure to a wood building environment does not have any adverse effects in rats.

• Clinical and Experimental Reproductive Medicine
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• v.39 no.4
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• pp.144-152
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• 2012

Objective: Concerns are growing about the decrease in male reproductive health. Caffeine is one of the popular nutrients that has been implicated as a risk factor for infertility. In the present study, we examined whether in utero and lactational exposure to caffeine affects the reproductive function of the offspring of rats. Methods: Pregnant rats received caffeine via drinking water during gestation (26 and 45 mg/kg) and lactation (25 and 35 mg/kg). Body and reproductive organ weight, seminiferous tubule diameter, germinal epithelium height, sperm parameters, fertility rate, number of implantations, and testosterone level of the offspring were assessed from birth to adulthood. Results: Significant dose-related decreases were observed in the body and reproductive organ weight, seminiferous tubule diameter, and germinal epithelium height of the offspring. Sperm density had declined significantly in offspring of the low-dose and high-dose groups, by 8.81% and 19.97%, respectively, by postnatal day 150. The number of viable fetuses had decreased significantly in females mated with male offspring of the high-dose group at postnatal days 60, 90, 120, and 150. There were also significant reductions in testosterone levels of high-dose group offspring from birth to postnatal day 150. Conclusion: It is concluded that maternal caffeine consumption impairs gonadal development and has long-term adverse effects on the reproductive efficiency of male offspring rats.

• Biomedical Science Letters
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• v.21 no.1
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• pp.15-22
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• 2015

Dexamethasone, a synthetic glucocorticoid (GC), is clinically administered to woman at risk for premature labor to induce fetal lung maturation. However, exposure to repeated or excess GCs leads to intrauterine growth restriction (IUGR) and subsequently increases risk of psychiatric and cardio-metabolic diseases in later life through fetal programming mechanisms. GCs are key mediators of stress responses, therefore, maternal nutrient restriction or psychological stress during pregnancy also causes negative impacts on birth and neurodevelopment outcome of fetuses, and other congenital defects, such as craniofacial and skeletal abnormalities. In this study, to examine the effect of prenatal stress on fetal skeletal development, dexamethasone (1 mg/kg [DEX1] or 10 mg/kg [DEX10] maternal body weight per day) was administered intraperitoneally at gestational day 7.5~9.5 and the skeletons were prepared from embryos at day 18.5. Seven out of eighteen (39%) embryos treated with DEX10 showed axial skeletal abnormalities in either the T13 or L1 vertebrae. In addition, examination of the sternum revealed that xiphoid process, the protrusive triangular part of the lower end of the sternum, was bent more outward or inward in DEX group embryos. In conclusion, our findings suggest a possible link to the understanding of the effect of uterine environment to the fetal skeletal features.

• Childhood Kidney Diseases
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• v.27 no.2
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• pp.121-126
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• 2023

The administration of angiotensin type 2 receptor blockers (ARBs) during pregnancy is known to cause ARB fetopathy, including renal insufficiency. We aimed to analyze the outcomes of two patients who survived ARB fetopathy and perform an accompanying literature review. Case 1 was exposed antenatally from a gestational age of 30 weeks to valsartan because of maternal pregnancy-induced hypertension. The patient presented with oliguria immediately after birth, and renal replacement therapy was administered for 24 days. Seven years after birth, renal function was indicative of stage 2 chronic kidney disease (CKD) with impaired urinary concentration. Case 2 had a maternal history of hypertension and transient ischemic attack and was treated with olmesartan until 30 weeks of pregnancy. Renal replacement therapy was performed for 4 days since birth. After 8 years, the patient is with CKD stage 2, with intact tubular function. Recent reports suggest that ARB fetopathy might manifest as renal tubular dysgenesis and nephrogenic diabetes insipidus, in contrast to mild alterations of glomerular filtration. Tubular dysfunction may induce CKD progression and growth retardation. Patients with ARB fetopathy should be monitored until adulthood. The ARB exposure period might be a critical factor in determining the severity and manifestations of fetopathy.

• Proceedings of the Korean Environmental Health Society Conference
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• 2005.06a
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• pp.73-83
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• 2005

Higher methylmercury (MeHg) accumulation and susceptibility to toxicity in the fetus than in the mother at parturition is well known. However, the difference in MeHg exposure to fetus and offspring throughout gestation and suckling is not well established. In the human, the effects of MeHg exposure on pregnant and breast-feeding women remain an important issue for elucidation, especially those of continuous uptake in high-fish-consumption populations. The purpose of this paper was to evaluate the difference in MeHg exposure to fetus and offspring throughout gestation and lactation using our recent animal and human studies data. In the animal study, adult female rats were given a diet containing 5 ${\mu}$g/g Hg (as MeHg) for 8 weeks. Then they were mated and subsequently given the same diet throughout gestation and suckling. On embryonic days 18, 20, 22 and at parturition, the concentrations of Hg in the brains of fetus were approximately 1.5-2.0 times higher than those in the mothers. However, during the suckling period Hg concentrations in the brain rapidly declined to about 1/10 of that during late pregnancy. Hg concentrations in blood also decreased rapidly after birth. In human study, Hg concentrations in red blood cells (RBCs-Hg) in 16 pairs of maternal and umbilical cord blood samples were compared at birth and 3 months of age after parturition. RBCs-Hg concentration in the umbilical cords was about 1.6 times higher than those in the mothers at parturition. However, all the infants showed declines in Hg concentrations throughout the breast-feeding period. The Hg concentration in RBCs-Hg at 3 months of age was about half that at birth. Both the animal and human studies indicated that MeHg exposure to the fetus might be especially high but it dramatically decreases during the suckling period. Therefore, close attention should be paid to the gestation rather than the breast-feeding period to avoid the risk of MeHg to human infants.

• Journal of Ginseng Research
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• v.46 no.1
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• pp.62-70
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• 2022

Background: Maternal Toxoplasma gondii (T. gondii) infection during pregnancy has been associated with various mental illnesses in the offspring. Ginsenoside Rh2 (GRh2) is a major bioactive compound obtained from ginseng that has an anti-T. gondii effect and attenuates microglial activation through toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) signaling pathway. GRh2 also alleviated tumor-associated or lipopolysaccharide-induced depression. However, the effects and potential mechanisms of GRh2 on depression-like behavior in mouse offspring caused by maternal T. gondii infection during pregnancy have not been investigated. Methods: We examined GRh2 effects on the depression-like behavior in mouse offspring, caused by maternal T. gondii infection during pregnancy, by measuring depression-like behaviors and assaying parameters at the neuronal and molecular level. Results: We showed that GRh2 significantly improved behavioral measures: sucrose consumption, forced swim time and tail suspended immobility time of their offspring. These corresponded with increased tissue concentrations of 5-hydroxytryptamine and dopamine, and attenuated indoleamine 2,3-dioxygenase or enhanced tyrosine hydroxylase expression in the prefrontal cortex. GRh2 ameliorated neuronal damage in the prefrontal cortex. Molecular docking results revealed that GRh2 binds strongly to both TLR4 and high mobility group box 1 (HMGB1). Conclusion: This study demonstrated that GRh2 ameliorated the depression-like behavior in mouse offspring of maternal T. gondii infection during pregnancy by attenuating the excessive activation of microglia and neuroinflammation through the HMGB1/TLR4/NF-κB signaling pathway. It suggests that GRh2 could be considered a potential therapy in preventing and treating psychiatric disorders in the offspring mice of mothers with prenatal exposure to T. gondii infection.

• Proceedings of the KSAR Conference
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• 2003.06a
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• pp.31-31
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• 2003

The incidence of reproductive abnormalities in the male has been reported to have increased during the past 50 years. These changes may be attributable to the presence of chemical with oestrogenic activity in our environment. Present study was carried out to determine the effects of maternal exposure to xenoestrogens on the testicular development and on the transcriptional expression of the steroidogenic enzyme and subunits of inhibin/activin in testis of male offspring. Pregnant female mice were administrated with 4-tert-octylphenol (OP; 2, 20, 200mg/kg), Bisphenol A (BPA; 2, 20, 200$\mu\textrm{g}$/kg), $\beta$-estradiol 17-valerate (EV; 2$\mu\textrm{g}$/kg) or vehicle (CV; corn oil) during gestational days 11 to 17. Offsprings were sacrificed on gestational day 18 (fetal 18) and neonatal day 7. Body weights were significantly increased in groups treated with all doses of OP and BPA. Maximum seminiferous tubules diameter on gestational day 18 were not changed in any treatment group, however, they were significantly increased on the neonatal day 7 in the group treated with low-dose of OP (2 mg/kg) and BPA (2 $\mu\textrm{g}$/kg). Increased expression of the P450$_{17a}$-hydroxylase dehydrogenase (P450$_{17a}$), 3$\beta$-hydroxylase dehydrogenase (3$\beta$-HSD), and 17$\beta$-hydroxylase dehydrogenase (17$\beta$-HSD) on gestational day 18 were observed in the groups treated with 2 or 20 mg/kg of OP. However, expression of the steroidogenic enzymes were not changed in the groups treated with all the doses of BPA. In contrast with the results from fetal testis, no expressional changes of these enzymes was found in all the OP-treated group and increased expression of inhibin/activin $\beta$B subunit mRNA were obseued in the 200 $\mu\textrm{g}$/kg BPA-treated group in the neonatal day 7. These results suggest that gestational exposure to low level of xenoestrogen causes a stimulatory effects on the transcriptional expressions of steroidogenic enzymes and subunits of inhibin/activin and on the seminiferous tubule development by their estrogen-like actions.ons.