The effect of radiation on cells is usually exerted through the formation of ROS.
Although single doses of radiation used for diagnostic purposes or therapeutic treatment are relatively low, small changes on the molecular and cellular level may accumulate upon repeated exposure and result in delayed long-term defects.
Oxygen concentration and differentiation state are important in studies of disease mechanisms, particularly of age-related diseases such as neurodegenerative AD (Alzheimer s disease). Although exact cause(s) of AD are still unknown, one of the players is Aβ peptide. However, the implication of different aggregation states of the peptide (fibrillized or disaggregated to monomers and oligomers) is largely debated.
Monomers and small oligomers of Aβ peptide are recently proposed to be involved in damage of neurons, instead of extracellular Aβ peptide plaques, since they interact with and even intercalate in cellular membranes and the peptide is found inside neurons of AD patients. Lysosomal activity of sequestration and potential degradation of Aβ peptide is probably the first and most important defense mechanism of cells against Aβ peptide toxicity.
Although effects of irradiation and Aβ peptide share some similarities, such as induction of inflammation linked with neurodegeneration, these two stressors probably affect different cellular pathways and result in different cellular responses.