• Title/Summary/Keyword: Antifouling paints

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Pyrolysis Treatment for TBT Paint Waste from Ship (선박용 TBT 방오페인트 폐기물의 열분해 처리)

  • Park, Sang-Ho;Kim, In-Soo;Song, Young-Chae;Woo, Jung-Hui;Kim, Dong-Geun
    • Journal of Navigation and Port Research
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    • v.27 no.4
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    • pp.449-454
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    • 2003
  • Bans on TBT based antifouling paints have been drafted since 1998 by meetings 42, 43, 45 and 46 for the MEPC(Marine Environmental Protection Committee) of the international Maritime Organization, and decided finally at a Diplomatic Conference of the IMO in October 2001. It was a key issue that there should be a global prohibition on the presence of organo-tin compounds in ships by 1 Jan. 2008. TBT Paint Wastes from ship have been produced by vast quantity since 2003. This paper suggests a method to design Treatment System for TBT Paint Waste from Ship. The organotion compound was dissolved by heating, and the organic matters was oxidized and turned into inorganotins, then they were stabilized in the end. At 500^{\circ}C$, the organotin compound which heated for one hour was removed by 58%, and in 1000^{\circ}C$ the organotin compound was treated by 99.9% after and hour of heating treatment.

Mechanisms of Tributyltin-induced Leydig Cell Apoptosis (유기주석화합물이 웅성생식세포주에 미치는 영향)

  • Lee, Kyung-Jin;Kim, Deok-Song;Ra, Myung-Suk;Wui, Seong-Uk;Im, Wook-Bin;Park, Hueng-Sik;Lee, Jong-Bin
    • Environmental Analysis Health and Toxicology
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    • v.18 no.2
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    • pp.89-94
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    • 2003
  • Tributyltin (TBT) used world-wide in antifouling paints for ships is a widespread environmental pollutant and cause reproductive organs atrophy in rodents. 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 DNA fragmentation induced by TBT in the rat leyding cell line, R2C. Effects of TBT on intracellular Ca$\^$2+/ level and reactive oxygen species (ROS) were investigated in R2C cells by fluorescence detector. TBT significantly induced intracellular Ca$\^$2+/ level in a time-dependent manner. The rise in intracellular Ca$\^$2+/ level was followed by a time-dependent generation of reactive oxygen species (ROS) at the cytosol level. Simultaneously, TBT induced the release of cytochrome c from the mitochondrial membrane into the cytosol. Furthermore, ROS production and the release of cytochrome c were reduced by BAPTA, an intracellular Ca$\^$2+/ chelator, indicating the important role of Ca$\^$2+/ in R2C during these early intracellular events. In addition, Z-DEVD FMK, a caspase-3 inhibitor, decreased apoptosis by TBT. Taken together, the present results indicated that the apoptotic pathway by TBT might start with an increase in intracellular Ca$\^$2+/ level, continues with release of ROS and cytochrome c from mitochondria, activation of caspases,and finally results in DNA fragmentation.