The Cytotoxic Mechanisms of Bacillus thuringiensis $\delta$-endotoxin, a Bioinsecticide : Effect on $K^+$ Channel of Insect Cell Lines.

  • Seo, Young-Rok (Department of Agricultural Biology and Graduate School of Biotechnology, College of Natural Resources, Korea University, Toxicology Laboratory, Doping control Center, Korea Institute of Science and Technology) ;
  • Han, Sung-Sik (Department of Agricultural Biology and Graduate School of Biotechnology, College of Natural Resources, Korea University) ;
  • Yu, Yong-Man (Kyungnong Kyungju Institute) ;
  • Lee, Jun-Jae (Department of Agricultural Biology and Graduate School of Biotechnology, College of Natural Resources, Korea University) ;
  • Ryu, Jae-Chun (Toxicology Laboratory, Doping control Center, Korea Institute of Science and Technology)
  • 발행 : 1996.12.01

초록

The cytotoxicological effect of Bt 1-endotoxin, well-known as a bioinsecticide, was investigated on ion channel of insect cell lines. This study attempted to evaluted the specificity by simple experiment to measure the cell swelling using lepidopteran cell lines in isotonic solution containing only one cation. Cell swelling was stimulated in KCI-sucrose isotonic solution as well as TC-100 media containg in solubilized crystal 5-endotoxin. It suggested that the cell swelling by Bt toxin have a relation to K+ channel. The cell swelling may be due to the stimulation K+ influx and simultaneously the penetration of H2O induced by Bt toxin, because the stimulation of swelling was observed with the solubilized toxin in KCI-sucrose isotonic solution, but not in sucrose isotonic solution. Moreover the specific K+ channel blocker, such as 4-arnjnopyrimidine(4-AP) and ouabain, showed the significant effect on the cell swelling induced by Bt toxin. The increasement of the cell swelling induced by 4-AP suggested to be caused by the block of K+ efflux through K+ leak channels. The inhibition of cell swelling by ouabain, which is the well-known inhibitor of Na+, K+-ATPase, suggested to be due to decreasement of K+ influx following diminishment of Na+, K+-ATPase activities.

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