Cadmium is a heavy metal causing toxicity especially in kidney
cells. The toxicity is linked also with enhanced oxidative stress
leading to cell death. On the other hand, our recent experiments
have shown that an increase of total intracellular dehydrogenases
activity can also occur in kidney cells before declining until cell
death. The aim of the present study, therefore, was to evaluate
this transient enhancement in cell viability after cadmium
treatment. The human kidney HK-2 cell line was treated with
CdCl2 at concentrations 0-200 µM for 2-24 h and intracellular
dehydrogenase activity was tested. In addition, we measured
reactive oxygen species (ROS) production, glutathione levels,
mitochondrial membrane potential, and C-Jun-N-terminal kinase
(JNK) activation. We found that significantly increased
dehydrogenase activity could occur in cells treated with 25, 100,
and 200 µM CdCl2. Moreover, the results showed an increase in
ROS production linked with JNK activation following the
enhancement of dehydrogenase activity. Other tests detected
no relationship with the increased in intracellular dehydrogenase
activity. Hence, the transient increase in dehydrogenase activity
in HK-2 cells preceded the enhancement of ROS production and
our finding provides new evidence in cadmium kidney toxicity.