• Proceedings of the Korean Society of Toxicology Conference
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• 2003.05a
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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)

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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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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• v.32 no.1
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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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• v.18 no.2
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• pp.95-100
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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). As the results, the potent leyding cell activator LH increased testosterone production compared to the control. DDT exposure significantly decreased testosterone production in R2C cell and DDT alone affected T reduction in a dose-dependent manner in R2C cell slightly. In addition, DDT was found to increase aromatase activity in R2C cell in a dose dependent manner. In order to assess whether the suppressive effects of DDT on LH-inducible testosterone production might be influenced by the ER, ICI 182.780, a pure antiestrogen, was used, and it was found that these inhibitory effects of DDT were antagonized by ICI 182.780, implying that the ER mediates the suppressive effects of DDT. Furthermore, the inducible effects of DDT on aromatase 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 LH-inducible testosterone production in R2C is mediated through aromatase. However, the precise mechanisms by which DDT enhance in leyding cell remains unknown. The current study suggests the possibility that DDT might act as a modulator aromatase gene transcription.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2003.10a
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• pp.137-137
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• 2003

• Korean Journal of Environmental Agriculture
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• v.39 no.2
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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.

• Korean Journal of Environmental Biology
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• v.21 no.3
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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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• v.28 no.1
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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.