• Development and Reproduction
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• v.25 no.1
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• pp.15-24
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• 2021

Benzo[a]pyrene (B[a]P) is a potent carcinogen and is classified as an endocrine-disrupting chemical. In mammalian testes, Sertoli cells support spermatogenesis. Therefore, if these cells are negatively affected by exposure to xenotoxic chemicals, spermatogenesis can be seriously disrupted. In this context, we evaluated whether mouse testicular TM4 Sertoli cells are susceptible to the induction of cytotoxicity-mediated cell death after exposure to B[a] P in vitro. In the present study, while B[a]P and B[a]P-7,8-diol were not able to induce cell death, exposure to BPDE resulted in cell death. BPDE-induced cell death is accompanied by the activation of caspase-3 and caspase-7. Depolarization of the mitochondrial membrane and cytochrome c release from mitochondria were observed in benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE)-treated cells. These results indicate that TM4 cells are susceptible to apoptosis in a caspase-dependent manner. Western blot and reverse transcription-polymerase chain reaction (RT-PCR) analyses showed that aryl hydrocarbon receptor (AhR) expression was almost undetectable in TM4 cells and that its expression was not altered after B[a]P treatment. This indicates that TM4 cells are nearly AhR-deficient. In TM4 cells, the CYP1A1 protein and its activity were not present. From these results, it is clear that AhR may be a prerequisite for CYP1A1 expression in TM4 cells. Therefore, TM4 cells can be referred to as CYP1A1-deficient cells. Thus, TM4 Sertoli cells are believed to have a rigid and protective cellular machinery against genotoxic agents. In conclusion, it is suggested that tolerance to B[a]P cytotoxicity is associated with insufficient AhR and CYP1A1 expression in testicular Sertoli cells.

• Korean journal of applied entomology
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• v.44 no.2
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• pp.97-108
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• 2005

Samples of water, soil, and sediment were taken from 10 streams near Andong, Korea in May 2004. To assess the degree of environmental pollution of each stream, chemical pollutants such as total notrogen (T-N), total phosphorus (T-P), chemical oxygen demand (COD), heavy metals, organophosphorus pesticides, organochlorine pesticides, and dioxin-like PCB congeners were analyzed by standard process tests or U.S. EPA methods. In addition, biomarkers originated from insect immune systems of beet armyworm, Spodoptera exigua, were used to analysis of the environmental samples. Except Waya-chun stream showing T-N content of 9.12 mg/L, most streams were contaminated with relatively low levels of overall pollutants in terms of T-N, T-P, and COD, compared to their acceptable environmental levels designated by the Ministry of Environment. Contents of Pb and Cd in samples of each stream were much lower than environmentally permissible levels. However, several times higherconcentrations of Pb and Cd were found in locations at Mi-chun, Kilan-chun, and Hyunha-chun streams, in comparison with other streams. Diazinon, parathion, and phenthoate compounds among organophosphorus pesticides were detected as concentrations of 0.19, 0.40, and $1.13\;{\mu}g/g$, respectively, from soil sample collected in the vicinity of Mi-chun stream. On the other hand, 16 organochlorine pesticides and 12 dioxin-like PCB congeners, known as endocrine disrupting chemicals, selected in this study were not found above the limit of detection. Biomarker analyses using insect immune responses indicated that Waya-chun stream was suspected as exposure to environmental pollutants. Limitation and compensation of both environmental analysis techniques are discussed.

• Development and Reproduction
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• v.14 no.4
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• pp.297-306
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• 2010

Tributyltin (TBT), an endocrine disrupting chemical, has been reported to decrease testicular function by causing apoptosis in the testis, but this mechanism is not fully understood. Thus, in this study we examined whether TBT induces adipogenesis of the Leydig cells to find out the correlation between adipogenesis and apoptosis in the testis. Three week old SD male rats were orally administrated with sesame oil, 1 mg/kg of TBT, or 10 mg/kg of TBT daily for 1 week and weighed after administration. The testes obtained on day 8 were weighed and stained with BODIPY and TUNEL kit. Using total RNA extracted from the isolated Leydig cells, adipogenesis and apoptosis-related genes were analyzed by real-time PCR. The testicular weights of the rats treated with 10 mg/kg TBT were significantly decreased compared to those in the control rats treated with sesame oil. As a result of BODIPY staining, the number of Leydig cells stained with BODIPY was increased in the rats treated with 10 mg/kg TBT compared with the control rats. Similar to BODIPY staining results, the TUNEL assay showed that the apoptosis of Leydig cells was increased in TBT treated rats. The results of the gene expression analysis in the Leydig cells showed that the expression of adipogenesis-related genes (PPAR${\gamma}$, aP2, Perilipin, CD36) and apoptosis-related genes (TNFRSF1A, TNFSF10) was increased after TBT administration. The present study demonstrates that TBT induces the expression of adipogenesis-related and apoptosis-related genes in the Leydig cells leading to adipogenesis and apoptosis in the testes. These results suggest that the dysfunction of Leydig cells by TBT exposure may cause a loss in testicular function.