ABSTRACT
Oxidative stress is a major factor contributing to endothelial cell damage. Single-wall carbon nanotubes (SWCNTs) have oxidative properties; however, the oxidative effects of SWCNTs on endothelial cells are not fully understood. In the present study, we investigated the effects of oxidative stress induced by SWCNTs on rat aortic endothelial cells (RAECs). Various markers of cellular damage were assessed, such as biochemical and ES immunity indexes, and DNA and protein damage. Our findings suggest that RAEC endured oxidative damage following SWCNT exposure. Specifically, after SWCNTs exposure, non-enzymatic antioxidant glutathione was activated prior to superoxide dismutase activation in order to defend against oxidative stress. Additionally, it was found that as SWCNT concentration increased, so did the stress protein, heme oxygenase-1 (HO-1), expression levels. These changes may induce RAEC damage, and result in many serious diseases.
Subject(s)
Aorta/cytology , Endothelial Cells/drug effects , Nanotubes, Carbon/toxicity , Oxidative Stress/drug effects , Animals , Cells, Cultured , Comet Assay , DNA Damage , Dose-Response Relationship, Drug , Fluorescent Antibody Technique , Gene Expression Regulation/drug effects , Heme Oxygenase-1/genetics , Heme Oxygenase-1/metabolism , Porins , Rats , Reactive Oxygen Species/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Superoxide Dismutase/metabolism , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolism , Tumor Suppressor Protein p53/genetics , Tumor Suppressor Protein p53/metabolismABSTRACT
The use of nano-sized materials offers exciting new options in technical and medical applications. Single-walled carbon nanotubes are emerging as technologically important in different industries. However, adverse effects on cells have been reported and this may limit their use. We previously found that 200µg/mL of single-walled carbon nanotubes induce apoptosis in rat aorta endothelial cells. The current study aimed to determine the signaling pathway involved in this process. We found that reactive oxygen species generation was involved in activation of the mitochondria-dependent apoptotic pathway. The finding of apoptosis was supported by a number of morphological and biochemical hallmarks, including chromatin condensation, internucleosomal DNA fragmentation, and caspase-3 activation. In conclusion, our results demonstrate that single-walled carbon nanotubes induce apoptosis in rat aorta endothelial cells and that reactive oxygen species are involved in the mitochondrial pathway.
