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(41-13) Effects of cadmium chloride on the glucose transport in L6 myotube. Moon, Chang-Kiu1, Kang, Dong-Hee1, Lee, Kiseon1, Kwon, Somee*,1, Chae, Sang-Ho1, 1 College of Pharmacy, Seoul National University, San 56- 1, Shillim-Dong, Kwanak-Gu, Seoul, South Korea, Seoul, Republic of Korea ABSTRACT- This study was aimed to know the effect of cadmium chloride(CdCl2) on glucose transport in L6 myotube and its action mechanism. CdCl2 increased the 2-DOG uptake 2 and 2.4 fold at 10 and 25 Key words: Cadmium Chloride, glucose transport, L6-myotube, glutathione |
M respectively. To investigate the mechanism of glucose transport-stimulation induced by CdCl2, the wortmanin and PD98059 were used as PI3K(phosphatidylinositol 3-kinase) inhibitor and MAPK inhibitor respectively, in which 2-DOG uptake was not affected. This fact suggest that CdCl2 induced 2-DOG uptake may not be concerned to the insulin signalling pathway. Wheras nifedipine, a calcium channel blocker, and trifluoperazine, a calmodulin inhibitor, were found to inhibit the stimulted 2-DOG uptake by CdCl2. In addition, we also measured the ROS(reactive oxygen species) production and GSH level in L6 myotube to investigate the correlation between the glucose uptake and ROS. CdCl2 increased ROS generation approximately 1.5 fold and changed the cellular GSH level, but GSSG/GSH ratio was not changed. CdCl2-stimulated 2-DOG uptake and ROS generation were inhibited by N-acetylcystein. And BSO pretreatment, a potent inhibitor of 
-GCS, resulted in the dramatic decrease of 2-DOG uptake and also the increase of the sensitivity to cadmium cytotoxicity. The obtained results suggest that CdCl2-stimulated glucose uptake might be based on the activation of antioxidant defense mechanism of the cells.