CrossRef Real-time in vivo analysis of murine cells reveals autophagic flux defects before onset of autoimmune diabetes Olha Melnyk, Charanya Muralidharan, Bryce E
To date, it has been observed that the treatment with this kind of antitumor agents causes ROS generation, mitochondrial dysfunction (including frataxin deficiency, mitochondrial DNA damage and defective components of ETC), loss in antioxidant enzymes, ion channels disturbances and nerve tissue damage (protein carbonylation and lipid peroxidation) (Areti et al., in vitro and in vivo biochemical effects after exposure to high concentrations of oxaliplatin, including neuronal activation of the purinoreceptor subtype 7, ROS and NO production, lipid peroxidation, loss of mitochondrial transmembrane potential and further apoptosis via caspase 3 activation
This fragment oligomerizes and inserts into the plasma membrane, forming pores that disrupt membrane integrity, increase ion influx, and lead to cell swelling and eventual rupture ( Pyroptosis can be initiated via two pathways: classical and non-classical
Role of Alcohol in the Regulation of Iron Metabolism