Cell death following

The oxidant function of pro-apoptotic protein Bax was investigated through heterologous expression in yeast. Direct measurements of fatty acid content show that Bax-expression induces oxidation of mitochondrial lipids. This effect is prevented by the coexpression of Bcl-xL. The oxi-dation actually could be followed on isolated mitochondria as respiration-induced peroxidation of polyunsaturatedcis-parinaric acid and on whole cells as the increase in the amount of thiobarbituric acid-reactiveproducts. ...

11p tumor12 22-04-2013 37 2   Download

Exposure of mammalian cells to oxidant stress causes early (iron catalysed) lysosomal rupture followed by apoptosis or necrosis. Enhanced intracellular production of reactive oxygen species (ROS), presumably of mitochondrial origin, is also observed when cells are exposed to nonoxidant pro-apoptotic agonists of cell death. We hypothesized that ROS generation in this latter case might promote the apoptotic cascade and could arise from effects of released lysosomal materials on mitochondria.

9p tumor12 20-04-2013 30 1   Download

Oxidative stress, followed by the apoptotic death of pancreaticbcells, is considered to be one of causative agents in the evolution of the type 2 dia-betic state; therefore, the protection ofbcells can comprise an efficacious strategy for preventing type 2 diabetes. In the present study, RIN-m5F cells (i.e. the rat insulinoma bcell line) were stimulated with streptozotocin, resulting in a time- and concentration-dependent release of lactate dehydrogenase.

10p vinaphone15 28-02-2013 33 2   Download