Radiotherapy results in DNA damage, the most lethal form of which is a double-strand break (Willers et al, 2004).
DNA double strand breaks, the most lethal lesions widely considered to be responsible for radiation-induced cell death are repaired by both homologous recombination (HR) and non-homologous end joining (NHEJ) in a proliferating mammalian cell population.
When produced in excess of cellular anti-oxidant capacity, ROS are known to induce, apart from other damages, DNA double stand breaks (DSB), the most lethal form of DNA damage.
The most lethal DNA lesion caused by ionizing radiation is double-strand breaks.
H2AX is phosphorylated by ATM kinase in response to DNA double-strand breaks (DSBs; the most lethal lesion); this event results in the recruitment of downstream repair factors into a microscopically visible focus [ 48, 49].
DNA double-strand breaks (dsbs) are the most lethal form of cellular DNA damage, and are major IR-induced DNA lesions (Jeggo, 1998a).
Among the various forms of DNA damage induced by ionising radiation (IR), DNA double-strand breaks (Dsb) are the most lethal.
Of the various type of damage that arise within the cell, DNA double strand (DSBs) are considered as the most lethal form of DNA damage, which, if left unrepaired will lead to cell death [6], [7].
Ionizing radiation induces multiple types of DNA damage, but double strand breaks are considered to be the most lethal [ 33].
At the cellular level, DNA double strand breaks (DSBs) are considered as the most lethal lesions and sensitivity to ionising radiation will depend on the DSB repair efficacy possessed by the cell.
