Expression of NF-kappaB and ERK following heavy ion irradiation

Heavy ion irradiation of cells is known to increase cytotoxic, mutagenic, and carcinogenic effects. The increased biological effectiveness of these ions is as yet unexplained, except for the fact that, unlike gamma-radiation, they result in clustered damage. It is likely that the increased biological effectiveness is a consequence of altered signaling pattern, which in turn may be due to the difference in the nature of damage produced. Gamma irradiation has been known to activate both pro- and anti-apoptotic signaling pathways. Nuclear factor-kappaB (NF-kappaB) and extracellular signal regulated kinase (ERK) contribute to the survival of the irradiated cell. Moreover, NF-kappaB acts as a redox sensor. In the present study, we examined NF-kappaB and ERK as antiapoptotic factors that could lead to the inhibition of apoptosis and, consequently, to increased mutagenicity. Both these signaling factors show a fluctuation in their levels with time.