Walter Malorni

TL;DR: The results obtained by using different inhibitors of monoamine oxidases (MAO), i.e. pargyline, clorgyline and deprenyl, on mitochondrial integrity and apoptosis are described, representing the first demonstration that MAO‐A inhibitors may protect cells from apoptosis through a mechanism involving the maintenance of mitochondrial homeostasis.

TL;DR: The results suggest that oxidative imbalance in the peripheral blood of AD patients could mirror oxidative changes previously described in the central nervous system.

TL;DR: Results indicate that Carboxyfullerenes penetrate human keratinocytes, localize within mitochondria where they act both by scavenging free radicals and by protecting cells from apoptosis.

TL;DR: It is suggested that constitutive production of type I interferon by melanoma cells can act as an intracellular booster capable of increasing cell proneness to apoptosis by specifically modifying mitochondrial homeostasis and independently from the apoptotic cascade involved.

TL;DR: It is shown that other oxidant compounds, such as hydrogen peroxide, also induce a rapid down modulation of membrane TfR and that pretreatment of cells with the antioxidant, thiol supplier, N-acetylcysteine inhibits the downmodulation of these receptors elicited by either menadione or hydrogenperoxide, suggesting the existence of a potentially important protective mechanism through which iron uptake is prevented in oxidatively imbalanced cells.