• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 춘계학술대회 논문집
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• pp.70-71
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• 2003

Dichlorodiphenyltrichloroethane (DDT), is a widespread environmental pollutant. In this study, we investigated the effect of DDT on testosterone production through aromatase and investigated its molecular mechanism in testicular leydig cell, R2C. We investigated that the effects of DDT on testosterone production and its effects on aromatase activity in R2C cell by radio immunoassay (RIA). (omitted)

• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 추계학술대회
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• pp.137-137
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• 2003

Dichlorodiphenyltrichloroethane (DDT) is a widespread environmental pollutant. Earlier reports have demonstrated that DDT is an endocrine-active compound capable of affecting early-stage sexual differentiation in male rats. Experiments based on receptor binding affinity and receptor-mediated transcriptional activation have identified DDE as an androgen receptor antagonist.(omitted)

• Toxicological Research
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• 제32권1호
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• pp.21-33
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• 2016

Dichlorodiphenyltrichloroethane (DDT) is still used in certain areas of tropics and subtropics to control malaria and other insect-transmitted diseases. DDT and its metabolites have been extensively studied for their toxicity and carcinogenicity in animals and humans and shown to have an endocrine disrupting potential affecting reproductive system although the effects may vary among animal species in correlation with exposure levels. Epidemiologic studies revealed either positive or negative associations between exposure to DDT and tumor development, but there has been no clear evidence that DDT causes cancer in humans. In experimental animals, tumor induction by DDT has been shown in the liver, lung, and adrenals. The mechanisms of hepatic tumor development by DDT have been studied in rats and mice. DDT is known as a non-genotoxic hepatocarcinogen and has been shown to induce microsomal enzymes through activation of constitutive androstane receptor (CAR) and to inhibit gap junctional intercellular communication (GJIC) in the rodent liver. The results from our previously conducted 4-week and 2-year feeding studies of p,p'-DDT in F344 rats indicate that DDT may induce hepatocellular eosinophilic foci as a result of oxidative DNA damage and leads them to hepatic neoplasia in combination with its mitogenic activity and inhibitory effect on GJIC. Oxidative stress could be a key factor in hepatocarcinogenesis by DDT.

• Environmental Analysis Health and Toxicology
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• 제18권2호
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• pp.95-100
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• 2003

본 연구는 환경호르몬(endocrine disruptors)으로 분류되었으며, 제초제로 널리 사용되었던 Dichlorodiphenyltrichloroethane(DDT)가 설치류의 생식세포 중 Leydig 세포의 testosterone(T)생성억제 및 그 관련 작용메카니즘을 규명코자 수행되었다. 먼저 흰쥐의 웅성 생식세포주인 R2C세포에 T의 양 및 aromatase 활성도를 radio immunoassay (RIA)방법을 이용하여 측정하였다. 그 결과 R2C 세포에 황체형성호르몬(LH)를 처리하여 testosterone생성을 증가시킨 후, DDT를 처리한 군들은 대조군에 비하여 농도 의존적으로 T의 양은 감소하였으며, aromatase 활성도는 증가하였다. 또한 DDT자체만 처리한 군에서도 대조군에 비하여 testosterone의 생성이 감소하였다. 이러한 aromatase활성 증가가 estradiol receptor(ER)와의 상호 관련성을 확인하기 위해 ER antagonist인 ICI 182.780를 처리한 후 T의 양 및 aromatase 활성도를 측정한 결과 DDT에 의해 증가된 aromatase활성도가 ICI 182.780에 의해 다시 감소됨을 확인하였다. 또한 DDT에 의해 감소된 T의 양도 ICI 182.780에 의해 다시 회복되었다. In vivo실험으로 흰쥐에 DDT를 직접 투여한 후 정소 내 성 호르몬들을 측정해 본 결과 T의 양은 유의성 있게 감소하였으며, estradiol(E$_2$)의 양은 증가하였으며, aromatase 활성도도 감소하였다. 이러한 결과를 종합해 볼 때 DDT는 aromatase를 감소시키고, 이렇게 감소된 aromatase에 의해 testosterone 생성량을 억제하고, 이러한 DDT의 aromatase의 감소는 ER을 경유하는 것으로 추정할 수 있다.

• 한국환경성돌연변이발암원학회:학술대회논문집
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• 한국환경성돌연변이발암원학회 2003년도 추계학술대회
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• pp.137-137
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• 2003

• 한국환경농학회지
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• 제39권2호
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• pp.89-94
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• 2020

BACKGROUND: Persistent organic contaminants such as dichlorodiphenyltrichloroethane (DDT) are often found in agricultural soils decades after it was banned in Korea. This study uses hemoglobin and hemoglobin-containing blood meal to reduce the residual DDT in soil. METHODS AND RESULTS: Hemoglobin or blood meal with or without hydrogen peroxide (H₂O₂) was mixed with the DDT-spiked soil prepared for this study, and samples were taken over 14 d-degradation period to measure the residual DDT concentrations. With only hemoglobin, DDT was completely removed after 14 d, while with both hemoglobin and H₂O₂, 73%, on average, removal was observed. Similarly, the blood meal removed 73% of DDT, but with H₂O₂, the DDT removal was only 39%. The lower DDT removal in the presence of H₂O₂ can be attributed to the adverse effects of reactive species. Hemoglobin was more effective than blood meal for DDT removal in a given time; however, with additional blood meal injection, complete DDT removal was achieved. CONCLUSION: Overall, this study shows that the blood meal that is used as a fertilizer can potentially be used to remove residual contaminants such as DDT in agricultural soil.

• 환경생물
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• 제21권3호
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• pp.308-312
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• 2003

Various pesticides known or suspected to interfere with steroid hormone function were screened toy effects in leydig cells on catalytic activity and mRNA expression of aromatase. Dichlorodiphenyltrichloroethane (DDT) is a widespread environmental pollutant. In this study, we investigated the effect of DDT on testosterone production through aromatase activity and its molecular mechanism in testicular leydig cell, R2C by using radioimmunoassay (RIA). As the results, the potent leydig: cell activator LH increased testosterone production compared to the control. DDT exposure significantly decreased testosterone production in R2C cell. In addition, DDT was found to increase aromatase gene expression and activity in R2C cell in a dose dependent manner. In order to assess whether the suppressive effects of DDT on LH-inducible testosterone (T) production might be influenced by the ER, ICI 182.780 was used, and it was found that these inhibitory effects of DDT were antagonized by ICI 182.780, implying that the estrogen receptor (ER) mediates the suppressive effects of DDT. Furthermore, the inducible effects of DDT on aromatase gene expression might be influenced by the ER, ICI 182.780 was used, and it was found that these enhancing effects of DDT were antagonized by ICI 182.780, implying that the ER mediates the inducible effects of DDT. Our results indicated that DDT inhibition of luteinizing hormone (LH) -inducible T production in R2C cell is mediated through aromatase. However, the precise mechanisms by which DDT enhance in R2C cell remains unknown. The current study suggests the possibility that DDT might act as a modulator aromatase gene transcription.

• Ocean and Polar Research
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• 제28권1호
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• pp.45-56
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• 2006

This study investigated primarily the toxic effects of bis(tributyltin)oxide (TBT) and DDT (Dichlorodiphenyltrichloroethane) on the mortality of adult Acartia omorii and barnacle nauplii as well as the hatching rate of A. omorii. Subsequently, compound effects of TBT and DDT on the mortality of immature copepods were tested in order to assess whether or not synergistic influence existed in the mixture of sublethal concentration of two pollutants. Mortality of adult A. omorii increased as exposure concentration of DDT increased in the range of from 0.0001 to 1ppm. Egg hatching rate of the copepod showed no distinctive difference in the range between 0.1 and 10ppm, while barnacle nauplii showed abnormal motility of their appendages in the range of 0.0001 to 1 ppm. Mortality of adult A. omorii increased as TBT concentration increased within the range of 1 and 10 ppb, whereas egg hatching rate of the copepod showed no linear response to the same exposure range. Moreover, copepod nauplii were almost motionless even though copepod eggs hatched under the exposure condition of TBT $(0{\sim}10 ppb)$ and DDT $(0{\sim}10 ppm)$, respectively, suggesting that the nauplii are hard to develop into adult stage. On the basis of the sublethal concentration less than the 24-h $LC_{50}$, 0.001 ppm (DDT) and 2 ppb (TBT) were selected to confirm the compound effects of two pollutants on the mortality of immature copepods. Mortality of immature copepods under the condition of mixture of the two pollutants was higher than that in the single exposure condition. This result seems to indicate that synergistic effects of sublethal toxicants can make a more hazardous effect on the survival of immature copepods even though the concentration of single toxicant is not lethal to copepods in the marine environment.