• Proceedings of the PSK Conference
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• 2001.10a
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• pp.189.2-190
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• 2001

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2002.05a
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• pp.69-70
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• 2002

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.189.1-189.1
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• 2001

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.160.1-160.1
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• 2001

• Korean Journal of Environmental Biology
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• v.21 no.3
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• pp.303-307
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• 2003

Tributyltin (TBT) used world-wide in antifouling paints toy ships is a wide-spread environmental pollutant. At low doses, antiproliferative modes of action have been shown to be involved, whereas at higher doses apoptosis seems to be the mechanism of toxicity in reproductive organs by TBT. In this study, we investigated that the mechanisms underlying apoptosis induced by TBT in R2C cell. Effects of TBT on intracellular $Ca^{2+}$ level and reactive oxygen species (ROS) were investigated in R2C cells by fluorescence detector. TBT significantly induced intracellular $Ca^{2+}$ level in a time-dependent manner. The rise in intracellular $Ca^{2+}$ level was followed by a time-dependent generation of reactive oxygen species (ROS) at the cytosol level. Simultaneously, TBT induced the release of cytochrome c from the mitochondrial membrane into the cytosol. Furthermore, ROS production and the release of cytochrome c were reduced by BAPTA, an intracellular $Ca^{2+}$ chelator, indicating the important role of $Ca^{2+}$ in R2C during these early intracellular events. In addition, Z-DEVD FMB, a caspase -3 inhibitor, decreased apoptosis by TBT. Taken together, the present results indicated that the apoptotic pathway by TBT might start with an increase in intracellular $Ca^{2+}$ level, continues with release of ROS and cytochrome c from mitochondria, activation of caspases, and finally results in DNA fragmentation.

• Ocean Science Journal
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• v.40 no.2
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• pp.61-66
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• 2005

Benthic amphipod, Grandidierella japonica widely inhabits the Korean coastal waters and is developed as a standard test species for sediment toxicity tests. We exposed G. japonica to various pollutants including 4 kinds of inorganic metals (Ag, Cd, Cu and Hg), tributyltin [TBT], ammonia and 7 polycyclic aromatic hydrocarbon (PAH) compounds (acenaphthene, chrysene, fluoranthene, fluorene, naphthalene, phenanthrene and pyrene) to estimate the no observed effect concentration (NOEC) and the median lethal concentration (LC50) of each pollutant during the 96-hour acute exposure. Among all tested pollutants, TBT was most toxic to G. japonica, and Rg was most toxic among inorganic metals. The toxicity of pyrene to G. japonica was greatest among PAH compounds, followed by fluoranthene, phenanathrene, acenaphthene, fluorene and naphthalene. The toxicity of PAH compounds was closely related to their physico-chemical characteristics such as $K_ow$ and water solubility. G. japonica responded adequately to pollutant concentrations and exposure durations, and the sensitivity of G. japonica to various inorganic and organic pollutants was generally comparable to other amphipods used as standard test species in ecotoxicological studies, indicating this species can be applied in the assessment of environments polluted by various harmful substances.

• Journal of Aquaculture
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• v.21 no.3
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• pp.146-156
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• 2008

Tributyltin chloride(TBTCl) was administered through discrete immersion(2 hr each) from the $18^{th}-25^{th}$ day after hatching(dph). At the doses of 1, 2, 4 and 8 ${\mu}g/L$, the immersion at 2 ${\mu}g/L$ ensured 93% masculinization and the highest survival of 75% after the treatment. TBTCl acted as a growth suppressant and the magnitude of its suppression was stronger in females. During the 300 day experiment, it postponed sexual maturity of females from 120$^{th}$ dph in the control to 240$^{th}$ dph in the females treated at 8 ${\mu}g/L$. It reduced spawning frequency(22-3 times) and cumulative fecundity(1,632-19 eggs) by reducing the number of vitellogenic eggs. In the treated males too, it reduced sperm motility(100-68 sec); consequently, fertilizability of the sperm cells drawn from these males was also reduced from 88 to 43%. Progeny testing showed that the cross between males treated at>2 ${\mu}g/L$ and normal females generated the presumed 'homogametic' males. Both the treated 'homogametic' and 'heterogametic' males could induce the females to spawn fewer eggs than that of the normal males. A normal female somehow deducted the differences between the control, treated and sex reversed males; it preferred a normal male over a treated one, and a treated one over the sex reversed male.

• Development and Reproduction
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• v.15 no.4
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• pp.373-383
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• 2011

Tributyltin (TBT) is one of endocrine disrupters which are known as having similar function to sex steroid hormone inducing apoptosis in various tissues of rodents. Recently, it has been reported that TBT induces apoptosis in thymus causing the decreased thymic function, but little is known about the mechanism. To elucidate the mechanism, three-week-old SD female rats were orally administrated with TBT 1, 10, and 25 mg per body weight (kg) and sesame oil as a control for 7 days. On day 8, the thymi were obtained and weighed, and then the number of thymocytes was counted. We also performed H&E staining, TUNEL assay, and Annexin V flow cytometric analysis to examine the apoptosis rates and the structure in the thymus. Next, we investigated the adipogenesis and apoptosis-related mRNA expression levels in the thymi by real-time PCR. The thymic weight and the number of thymocytes were decreased by TBT in a dose-dependent manner. As a result of the H&E staining, the boundary between cortical and medullary area was blurred in the thymi of TBT treated rats compared to those of controls. In the results of TUNEL assay and Annexin V flow cytometric analysis, apoptosis rates in the thymus were increased after TBT treatment. The expression levels of thymic epithelial cell marker genes such as EVA, KGF, AIRE, and IL-7 were significantly decreased in the thymi of TBT treated rats, but $PPAR{\gamma}$, aP2, PEPCK, and CD36 were significantly increased. The expression of $TNF{\alpha}$ and TNFR1 as apoptosis-related genes also was significantly increased after TBT treatment. The present study demonstrates that TBT can increase the expression of adipogenesis and apoptosis-related genes leading to apoptosis in the thymus. These results suggest that the increased adipogenesis of thymus by TBT exposure might induce apoptosis in the thymus resulting in a loss in thymic immune function.

• 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.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2001.11a
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• pp.77-77
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• 2001