Antimony induces oxidative stress and cell death in normal hepatocytes

Antimony (Sb) accumulates in the liver which is one of the target organs for metal-mediated toxicity. Although toxicity of Sb was previously investigated, the precise mechanism of Sb-induced hepatotoxicity remains to be determined. The aim of this study was to examine the role of oxidative stress, and mitochondria in the induction of cell death by Sb. Our results showed that liver cell lysis induced by Sb is mediated by reactive oxygen species (ROS) formation, lipid peroxidation and decline of mitochondrial membrane potential (MMP). Antimony-induced ROS formation, lipid peroxidation and reduction of MMP were significantly diminished by antioxidants and ROS scavengers such as dimethyl sulfoxide and mannitol; mitochondrial permeability transition (MPT) pore sealing agents such as carnitine and trifluoperazine; and adenosine triphosphate (ATP) generator, L-glutamine. Antimony-induced ROS formation, lipid peroxidation and fall in MMP were potentiated by glutathione (GSH) depletion via n-bromoheptane. MPT pore sealing agents and ATP generator inhibited hepatotoxicity, indicating Sb-activated cell death via mitochondrial pathway. Pretreatment of hepatocytes with antioxidants and ROS scavengers also blocked cell death induced by Sb, whereas GSH depletion enhances Sb-induced cell death, suggesting that oxidative stress may be directly involved in the reduction of MMP. These findings contribute to a better understanding of the mechanisms that mediate Sb-induced cell death in isolated rat hepatocytes.     

Association between Blastocystis sp. infection and immunocompromised patients: a systematic review and meta-analysis

Environmental Science and Pollution Research - The significance of opportunistic infections in immunocompromised patients and the enigmatic pathogenicity of Blastocystis directed us to conduct the...