Single-walled carbon nanotubes (SWCNTs) and multiwalled carbon nanotubes (MWCNTs) are broadly applicable across a variety of industrial fields. Despite their usefulness in many different applications, oxidative stress-induced toxicity of SWCNTs and MWCNTs has not been widely investigated. The present study examined the effects of SWCNTs and MWCNTs on rat brain mitochondria using the 3,4 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and indices of reactive oxygen species (ROS), based on measurements of malondialdehyde (MDA), glutathione (GSH), and mitochondrial membrane potential. Based on the MTT assay, exposure to SWCNTs and MWCNTs decreased mitochondrial survival and viability in a dose-dependent manner. Findings also indicated that MWCNTs and SWCNTs could damage mitochondrial membranes and induce the formation of ROS, as indicated by increased levels of MDA and decreased GSH content. The results of this study suggest that SWCNTs and MWCNTs likely damage brain tissue mitochondria by increasing oxidative stress and possibly activating the apoptosis pathway as well as other pathways of cytotoxicity.
17 March 2018 in Journal of Cardiovascular and Thoracic Research
The relentlessly beating heart has the greatest oxygen consumption of any organ in the body at rest reflecting its huge metabolic turnover and energetic demands. The vast majority of its energy is produced and cycled in form of ATP which stems mainly from oxidative phosphorylation occurring at the respiratory chain in the mitochondria. A part from energy production, the respiratory chain is also the main source of reactive oxygen species and plays a pivotal role in the regulation of oxidative stress. Dysfunction of the respiratory chain is therefore found in most common heart conditions. The pathophysiology of mitochondrial respiratory chain dysfunction in hereditary cardiac mitochondrial disease, the aging heart, in LV hypertrophy and heart failure, and in ischaemia-reperfusion injury is reviewed. We introduce the practicing clinician to the complex physiology of the respiratory chain, highlight its impact on common cardiac disorders and review translational pharmacological and non-pharmacological treatment strategies.