A possible correlation between the growth rate and the extent of DNA damage induced by radiodecay in mouse lymphoma cells

Ribeiro, P. L.; Martinez, M.C.; Mitra, Raj S.

doi:10.1016/0006-291x(85)91665-1

Cited by 6 publications

(1 citation statement)

References 12 publications

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“…In a related study, based on the fact that prim ing doses of X -rays (with 4 ± 6 h interval) abolish th e H RS region (M arples and Joiner 1995), Koch an d G ian dom enico (1994a) com pared the elution of D N A of V79 cells irradiated with and without a prim ing dose (~2 G y, 4 h) but no m arked differences in elution pro® les were seen before repair (addition al dose of 2 G y) or after 1 h or 20-m in repair (~10 G y) suggesting that neither initial dam age nor its repair rate re¯ect th e IRR/H RS structure. It was noted th at the 14 C-label itself could act as a prim er, as w ith the adaptive response (Ribeiro et al 1985, Ikushim a 1987. O ur m ore recent studies h ave con® rm ed that 3 H and 14 C-labelled cells exhibit less or no hyper-radiosensitivity <0 .…”

Section: Sin Gle-strand Breaks As Inducers Of Increased Radioresistancementioning

confidence: 99%

Response of V79 cells to low doses of X-rays and negative-mesons: clonogenic survival and DNA strand breaks

Marples¹,

Adomat

Koch

et al. 1996

International Journal of Radiation Biology

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Mammalian cells are hypersensitive to very low doses of X-rays (< 0.2 Gy), a response which is followed by increased radioresistance up to 1 Gy. Increased radioresistance is postulated to be a response to DNA damage, possibly single-strand breaks, and it appears to be a characteristic of low linear energy transfer (LET) radiation. Here we demonstrate a correspondence between the extent of the increased radioresistance and linear energy transfer of 250 kVp X-rays and plateau and Bragg peak negative pi-mesons. The results support our hypothesis since the size of the increased radioresistant response appears to correspond to the number of radiation induced single-strand breaks. Furthermore, since survival prior to the increased radioresistant response (< 0.2 Gy) was LET-independent, these data support the notion that the increased radioresistant response may dictate the overall survival response to higher doses. However, while these data provide further circumstantial evidence for the involvement of DNA strand breaks in the triggering of increased radioresistance, more direct conclusions cannot be made. The data are not accurate enough to detect structure in the single-strand break profiles, the production of single-strand breaks being apparently linear with dose.

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Section: Sin Gle-strand Breaks As Inducers Of Increased Radioresistancementioning

confidence: 99%