出版社：Korean Society of Environmental Health and Toxicology
摘要：Cadmium is well known as a toxic metal and has insulin mimicking effects in rat adipose tissue. This study was undertaken to investigate the effect of CdCl2 on glucose transport and its mechanism in 3T3-L1 adipocytes. CdCl2 exhibits respectively 2.2 and 2.8 fold increases in the 2-deoxyglucose uptake when exposed to 10 and 25 µM of CdCl2 for 12 hr. To investigate the stimulating mechanism of glucose transport induced by CdCl2,Wortmannin and PD98059 were used respectively as PI3K inhibitor and MAPK inhibitor,which did not affect 2-DOG uptake. This results suggest that induced 2-deoxy-(1-3 H)-D-glucose (2-DOG) uptake by CdCl2 may not be concerned with the insulin signalling pathway. Whereas nifedipine,a calcium channel blocker inhibited the 2-DOG uptake stimulated by CdCl2. In addition,we also measured the increased production of Reactive oxygen substances (ROS) and glutathione (GSH) level in 3T3-L1 adipocytes to investigate correlation between the glucose uptake and increased production of ROS with H2DCFDA. CdCl2 increased production of ROS. Induced 2-DOG uptake and increased production of ROS by CdCl2 were decreased by N-acetylcystein (NAC). And L-buthionine sulfoximine (BSO) a potent inhibitor of γ-GCS, decreased of 2-DOG uptake. Also NAC and BSO changed the cellular GSH level,but GSH/GSSG ratio remained unchanged at 10,25 µM of CdCl2.
关键词：cadmium;3T3-L1 adipocytes;reactive oxygen species;glutathione;redox state
