• Journal of Environmental Health Sciences
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• v.28 no.2
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• pp.131-139
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• 2002

초기생애단계의 일본송사리를 실험어류로 사용하여 TCDD와 PCB 126의 생물농축정도를 비교 측정하였고, TCDD와 PCB 126의 체외 배설에 대한 동태학적 특성을 비교 분석하였다. 생물농축실험은 초기생애단계의 새끼치어 및 어린 물고기에 TCDD와 PCB 126을 여러 농도로 물에 용해시켜 96시간 동안 정체된 상태로 폭로시킨 후 생물농축계수(BCF)와 지방-표준화한 생물농축계수(BCF$_{L}$)를 측정하였다. TCDD와 PCB 126의 일본송사리 초기생애단계의 새끼치어 및 어린 물고기에서 측정된 96-h BCF값 및 96-h BCF$_{L}$값은 폭로된 농도와 상관없이 비슷하게 나타나 반면, 생체크기가 클수록 그 값은 작게 나타났다. 일본송사리 새끼치어, 어린 물고기, 성어의 생체 내 총 지방함량은 각각 5.7, 4.2, 4.6%로 측정되었다. 체외배설 동태실험은 어린 물고기에 TCDD와 PCB 126을 3가지 농도롤 물에 용해시켜 96시간 동안 정체된 상태로 폭로시킨 후, flow-through장치로 공급되는 맑은 물로 옮겨 42일간 사양하면서 0, 7, 14, 21, 28, 42일에 생체 내 TCDD와 PCB 126 잔류량을 측정하여 분석하였다. 배설은 1차 반응속도론적으로 이루어졌으며 한 구획모형보다 두 구획모형이 더 적합한 것으로 분석되었다. 두 구획모형을 사용한 분석에서 TCDD와 PCB 126의 체외배설 반감기(t$\frac{1}{2}$) 및 배설속도상수($\beta$)는 각각 27.2일과 32.3일 및 0.025/d와 0.021/d로 측정되었다.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2001.05a
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• pp.121-121
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• 2001

Studies were carried out to compare the bioconcentrations of TCDD and PCB 126 in different sizes of Japanese medaka, and to examine the whole body elimination kinetics of TCDD and PCB 126 in juvenile Japanese medaka. For bioconcentration studies, different sizes of fry and juvenile medaka were exposed statically to varying doses of waterborne TCDD and PCB 126 for 96 hours. (omitted)

• Proceedings of the Korean Society of Developmental Biology Conference
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• 2003.10a
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• pp.63-63
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• 2003

In an effort to uncover the spermatogenic impairment by the polychlorinated biphenyls (PCBs), the expression of tight junctions (TJs) genes important for the formation of the blood testis barrier (BTB) were examined following the 3,3',4,4',5-pentachloro biphenyl (PCB126) treatment in cultured neonatal testis in mice. At 4 days (D4) after 10 and 100 nM PCB126 treatment the expression of claudin-11 was significantly increased when compared with vehicle control. In contrast no difference in occludin and claudin-1 expression was found among the experimental group. On D8, 100 nM PCB126 significantly increased the expression of claudin-11 but not occludin and claudin-1. 1 uM PCB126 treatment significantly decreased expressions of occludin and ciaudin -1, suggesting the general toxic effect on the Sertoli cell. Because PCB126 does not alter the proliferative activity of spermatogenic cells and Sertoli cells in neonatal testis, it is likely that increase in the expression of claudin-11 by low dose of PCB126 may attribute to the alteration of the Sertoli cells differentiation in testis. It also emphasized that PCB126 might have differentially affected the transcription of TJ genes in Sertoli cells. In conclusion, this result suggests that the structure of TJ may be targeted by PCB126 in neonatal testis in mice and that co-PCB is potentially harmful to spermatogenesis by alteration of the development of BTB.

• The Korean Journal of Pesticide Science
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• v.20 no.3
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• pp.203-210
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• 2016

Polychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants, found in the many environments. PCBs exerts various toxicological effects, including endocrine-disrupting activity. Most researches with these toxicants performed with soil matrix with mixtures of congeners, namely Aroclor, while the biological activities have been tested with animals. However, studies with pure congeners are limited. In this study, 5 congeners were synthesized and their fates (bioaccumulation, degradation, kinetics) were studied in carrot-soil system. The soil half-lives of biphenyl, PCB-1, PCB-3, PCB-77, and PCB-126 were 20.2, 16.0, 11.6, 46.5, 198.0 days, respectively. In general, the longer half-lives were observed with the higher hydrophoicity of PCBs. Times, required for maxium accumulation of PCBs in carrot (Tmax) were 10-20 days for most congeners and the concentrations were 0.4-2.6 mg/kg. The concentrations of PCBs in carrot were kept as constant after Tmax, except PCB-126. The concentration ratio between carrot and soil after 90 days of treatment were 1.7, 8.1, 1.9, 1.8, and 5.9 for biphenyl, PCB-1, PCB-3, PCB-77, and PCB-126. Because of the increase of biomass, the total residual amount of PCBs in carrots however, increased till the end of experiment. The portions of PCB-126 in carrot were 1.1% of the soil residues at 90 days after planting.

• Animal cells and systems
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• v.15 no.3
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• pp.189-196
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• 2011

We investigated the in vitro effects of nonylphenol (NP) and 3,3',4,4',5-pentachlorobiphenyl (PCB126) on steroidogenesis in redlip mullet, Chelon haematocheilus, oocytes. In experiment 1, we investigated the effects of NP and PCB126 on steroid production from exogenous steroid precursors. Vitellogenic oocytes (0.75 mm in diameter) were incubated with 10 and 100 ng/ml NP or PCB126 with $[^3H]17{\alpha}$-hydroxyprogesterone as a precursor. The major metabolites produced were androstenedione, testosterone (T), estrone, and estradiol-$17{\beta}$ ($E_2$). Both NP and PCB126 increased T production and decreased $E_2$ production, except for 100 ng/ml PCB126. In experiment 2, oocytes (0.65-0.75 mm in diameter) were exposed to NP and PCB126 at different concentrations (0.01, 0.1, 1, 10, and 100 ng/mL). After the incubation, T and $E_2$ production was measured by radioimmunoassay. NP inhibited $E_2$ production at concentrations of 0.01 and 0.1 ng/ml in 0.75-mm-diameter oocytes. NP at 1 and 100 ng/mL stimulated T production, but had no observable effect on $E_2$ production. PCB126 treatment did not affect $E_2$ production at any of the concentrations tested. NP alone at 0.1 ng/mL resulted in a significant decrease in $E_2$ production in 0.65-mm-diameter oocytes. PCB126 did not show any significant effects on either T or $E_2$ production at all concentrations tested. These results suggest that NP acts like an antiestrogen at lower concentrations (0.01-0.1 ng/ml) in vitellogenic oocytes of redlip mullet.

• Journal of Environmental Science International
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• v.20 no.8
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• pp.987-995
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• 2011

Co-planar PCBs(polychlorinated biphenyls) of non-ortho are investigated in soil and ginseng on the North Gyeongbuk with HRGC/HRMS. PCB77 in soil on Yeongju and Sangju are detected 0.0007 pgTEQ/g and 0.0009 pgTEQ/g, respectively. PCB81 in soil on Yeongju and Sangju are detected 0.0113 pgTEQ/g and 0.0108 pgTEQ/g, respectively. Also PCB126 in soil on Yeongju and Sangju are detected 0.0907 pgTEQ/g and 0.0944 pgTEQ/g, respectively. But PCB169 in soil on Yeongju and Sangju is not detected. Total Co-planar PCBs of non-ortho in soil on Yeongju and Sangju are 0.1027 pgTEQ/g and 0.1061 pgTEQ/g, respectively. PCB77 in ginseng on Yeongju and Sangju are detected 0.0008 pgTEQ/g. Then PCB81 in ginseng on Yeongju and Sangju are detected 0.0104 pgTEQ/g and 0.0112 pgTEQ/g, respectively. But PCB126 in ginseng on Yeongju and Sangju are detected 0.0585 pgTEQ/g and 0.0579 pgTEQ/g, respectively. PCB169 in ginseng on Yeongju and Sangju is not detected. Total Co-planar PCBs of non-ortho in ginseng on Yeongju and Sangju are 0.0697 pgTEQ/g and 0.0700 pgTEQ/g, respectively. Relationship of PCBs in between soil and ginseng shown significance($R^2$ : 0.99).

• Toxicological Research
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• v.28 no.2
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• pp.107-112
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• 2012

Polychlorinated biphenyls (PCBs) are persistent and bioaccumulative environmental pollutants. Recently, it is suggested that neurotoxic effects such as motor dysfunction and impairment in memory and learning have been associated with PCB exposure. However, structure relationship of PCB congeners with neurotoxic effects remains unknown. Since PKC signaling pathway is implicated in the modulation of motor behavior as well as learning and memory and the role of PKC are subspecies-specific, we attempted to study the effects of structurally distinct PCBs on the total PKC activity as well as subspecies of PKC in cerebellar granule cell culture model. Cells were exposed to 0, 25 and 50 ${\mu}M$ of PCB-126, PCB-169, PCB-114, PCB-157, PCB-52 and PCB-4 for 15 min. Cells were subsequently analyzed by [$^3H$] phorbol ester binding assay or immunoblotted against PKC-${\alpha}$ and -${\varepsilon}$ monoclonal antibodies. While non-dioxin-like-PCB (PCB-52 and PCB-4) induced a translocation of PKC-${\alpha}$ and -${\varepsilon}$ from cytosol to membrane fraction, dioxin-like PCBs (PCB-126, -169, -114, -157) had no effects. [$^3H$] Phorbol ester binding assay also revealed structure-dependent increase similar to translocation of PKC isozymes. While PCB-4 induced translocation of PKC-${\alpha}$ and -${\varepsilon}$ was inhibited by ROS inhibitor, the pattern of translocation was not affected in presence of AhR inhibitor. It is suggested that PCB-4-induced PKC activity may not be mediated via AhR-dependent pathway. Taken together, our findings suggest that chlorination of ortho-position in PCB may be a critical structural moiety associated with neurotoxic effects, which may be preferentially mediated via non-AhR-dependent pathway. Therefore, the present study may contribute to understanding the neurotoxic mechanism of PCBs as well as providing a basis for establishing a better neurotoxic assessment.

• International Journal of Oral Biology
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• v.44 no.3
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• pp.115-123
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• 2019

Among the environmental chemicals that may be able to disrupt the endocrine systems of animals and humans are polychlorinated biphenyls (PCBs), a chemical class of considerable concern. PCB consists of two six-carbon rings linked by a single carbon bond, and theoretically, 209 congeners can form, depending on the number of chlorines and their location on the biphenyl rings. Furthermore, 3,3',4,4',5-pentachlorobiphenyl (PCB126) exposure also increases nitric oxide production and nuclear factor kappa-light-chain-enhancer of activated B cells binding activity in chondrocytes, thus contributing as an initiator of chondrocyte apoptosis and resulting in thymic atrophy and immunosuppression. This study identified whether cardiac and immune abnormalities from PCB126 were caused by the Kv1.3 and Kv1.5 channels. PCB126 did not affect either the steady-state current or peak current of the Kv1.3 and Kv1.5 channels. However, PCB126 right-shifted the steady-state activation curves of human Kv1.3 channels. These results suggest that PCBs can affect the heart in a way that does not block voltage-dependent potassium channels including Kv1.3 and Kv1.5 directly.

• Proceedings of the Ginseng society Conference
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• 2004.05a
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• pp.36-38
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• 2004

• Proceedings of the Ginseng society Conference
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• 2005.05a
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• pp.16-18
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• 2005