出版社：Korean Society of Environmental Health and Toxicology
摘要：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-deoxy- (1-3 H)-D-glucose (2-DOG) uptake 1.9 and 2.4 fold at 10 and 25 µM respectively. To investigate the stimulating-mechanism of glucose transport induced by CdCl2,the wortmannin and PD98059 were used as PI3K (phosphatidylinositol 3-kinase) inhibitor and MAPK inhibitor respectively,which did not affect 2-DOG uptake. This fact suggests that CdCl2 induced 2-DOG uptake may not be concerned to the insulin signalling pathway. Whereas nifedipine,a calcium channel blocker, and trifluoperazine,a calmodulin inhibitor,were found to inhibit the 2-DOG uptake stimulted 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 (25 µM) increased ROS generation approximately 1.5 fold and changed the cellular GSH level,but GSSG/GSH ratio remained unchanged. CdCl2- stimulated 2-DOG uptake and ROS generation were inhibited by N-acetylcystein. And BSO pretreatment,a potent inhibitor of γ-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 HMP shunt as an antioxidant defense mechanism of the cells.
