Nickel (II)-induced cytotoxicity and apoptosis in human proximal tubule cells through a ROS- and mitochondria-mediated pathway.

Nickel compounds are known to be toxic and carcinogenic in kidney and lung. In this present study, we investigated the roles of reactive oxygen species (ROS) and mitochondria in nickel (II) acetate-induced cytotoxicity and apoptosis in the HK-2 human renal cell line. The results showed that the cytotoxic effects of nickel (II) involved significant cell death and DNA damage.

Nickel(II)-induced oxidative stress, apoptosis, G2/M arrest, and genotoxicity in normal rat kidney cells.

In order to elucidate the effects of nickel (Ni) on oxidative stress, apoptosis, and genotoxicity in renal cells, the levels of intracellular oxidants, lipid peroxidation, apoptotic proteins, and DNA damage were measured in normal rat kidney (NRK) cells after nickel chloride (NiCl(2)) treatment. NiCl(2) appeared to increase the formation of the fluorescent oxidized compound (dichlorofluorescein, DCF) and levels of thiobarbituric acid-reactive substances (TBARS). In flow cytometric analysis, a rise in cell proportion in sub-G1 phase occurred in a concentration-dependent manner.