KMID : 0893320050200010075
|
|
Journal of Environmental Toxicology 2005 Volume.20 No. 1 p.75 ~ p.85
|
|
Effects of Cadmium on Glucose Transport in L6 Myocytes
|
|
Kang Dong-Hee
Khil Lee-Yong Park Kwang-Sik Lee Byung-Hoon Moon Chang-Kiu
|
|
Abstract
|
|
|
This study was aimed to know the effect of cadmium chloride (CdCl©ü) on glucose transport in L6 myotube and its action mechanism. CdCl©ü increased the 2-deoxy- (l-3H)-D-glucose (2-DOG) uptake 1.9 and 2.4 fold at 10 and 25 ¥ìM respectively. To investigate the stimulating-mechanism of glucose transport induced by CdCl©ü, 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 CdCl©ü 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 CdCl©ü. 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. CdCl©ü(25 ¥ìM) increased ROS generation approximately 1.5 fold and changed the cellular GSH level, but GSSG/GSH ratio remained unchanged. CdCl©ü stimulated 2-DOG uptake and ROS generation were inhibited by N-acetylcystein. And BSO pretreatment, a potent inhibitor of ¥ã-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 CdCl©ü-stimulated glucose uptake might be based on the activation of HMP shunt as an antioxidant defense mechanism of the cells.
|
|
KEYWORD
|
|
Cadmium, Glucose transport, Myocytes, ROS, GHS
|
|
FullTexts / Linksout information
|
|
|
|
Listed journal information
|
|
|
|