Palladium induced oxidative stress and cell death in normal hepatocytes

Abstract

Palladium (Pd) accumulates in many organs and renders many deleterious effects. Although the Pd toxicity has been documented, the precise mechanism of Pd toxicity still needs to be elucidated. In the current research, a hepatotoxicity mechanism of Pd has been investigated. Our findings clearly indicate that Pd induces reactive oxygen species (ROS) formation and oxidative stress, mitochondrial and lysosomal injury and finally cell death. These effects are reversed by antioxidants and ROS scavengers, mitochondrial permeability transmission [1] pore sealing agent, ATP progenitor, and lysosomotropic agent. Pretreatment of hepatocytes with ROS scavengers and MPT pore sealing agents reduced cell death which explains the role of oxidative stress and mitochondrial pathway of ROS formation in Pd hepatocytes cell toxicity. Overall, the results have distinctly determined the mechanism by which Pd-induced toxicity in the isolated rat hepatocytes.

Keywords: Palladium; rat hepatocytes; reactive oxygen species; mitochondria; lysosome.