MAPK activation is involved in cadmium-induced Hsp70 expression in HepG2 cells.

Cadmium is one of the most toxic elements to which man can be exposed at work or in the environment. By far, the most salient toxicological property of Cd is its exceptionally long half-life in the human body. Once absorbed, Cd accumulates in the human body, particularly in the liver and other vital organs.

NADPH oxidase and ERK1/2 are involved in cadmium induced-STAT3 activation in HepG2 cells.

The molecular mechanism of Cd-induced signal transduction is not well understood. The aims of this study were to determine the system that generates reactive oxygen species in response to Cd that contribute to intracellular signaling on the activation of the STAT3 pathway in HepG2 cells and to address the participation of STAT3 in the production of Hsp70. Cadmium induced a significant increase in STAT3 DNA-binding after 1h treatment.

Cadmium induces alpha(1)collagen (I) and metallothionein II gene and alters the antioxidant system in rat hepatic stellate cells.

The mechanism of cadmium-mediated hepatotoxicity has been the subject of numerous investigations, principally in hepatocytes. Although, some uncertainties persist, sufficient evidence has emerged to provide a reasonable account of the toxic process in parenchymal cells. However, there is no information about the effect of cadmium in other hepatic cell types, such as stellate cells (fat storing cells, Ito cells, perisinusoidal cells, parasinusoidal cells, lipocytes).