|
KMID : 0379520010170030215
|
|
한국독성학회지
2001 Volume.17 No. 3 p.215 ~ p.223
|
|
|
Apoptotic Signaling Pathway by Cadmium in Hepalclc7 cells
|
|
Oh Gyung-Jae
Youm Jung-Ho
|
|
|
Abstract
|
|
|
|
Cadmium is an ubiquitous toxic metal and chronic exposure to cadmium results in the accumulation of cadmium in the liver and kidneys. In contrast, acute exposure leads to damage mainly in the liver. Apoptosis induced by cadmium has been shown in many tissues in vivo and in cultured cells in vitro. However, the molecular mechanism of cadmium-induced apoptosis is not clear in hepatocyte. To investigate the induction of apoptosis in the hepatocyte, we used mouse hepatoma cell line, Hepalclc7 cells, and analysed the molecules that involved in cadmium-induced apoptosis. Cadmium induced the genomic DNA fragmentation, PARP cleavage, and activation of caspase-3 like protease. Caspase-9 cysteine protease was activated in a time-dependent manner but caspase-8 cysteine protease was not significantly activated in cadmium-treated Hepalclc7 cells. Cadmium also induced mitochondrial dysfunction including cytochrome c release from mitochondria, change oj mitochondrial membrane potential tranition, and tranlocation of Bax Protein into mitochondria. These results strong1y indicated that the signal Pathway of apoptotic death in cadmium-treated Hepalclc7 cells is modulated by caspase cascade via mitochondria.
|
|
|
KEYWORD
|
|
|
Cadmium, Apoptosis, Hepalclc7 cell, caspase-3, caspase-9, Cytochrome c, Bax
|
|
|
FullTexts / Linksout information
|
|
|
|
|
Listed journal information
|
|
 
|
|