Abstract

AbstractInterstrand crosslinks can be shown in phage T7 DNA after treatment by nitrogen mustard or DL‐diepoxybutane, but not after treatment by myleran. Lethality increases after an ethylmethanesulfonate or myleran treatment; this increase is related to the increase of depurinations. Lethality first increases after the nitrogen mustard treatment, then decreases and finally increases again. Crosslinks account for the whole lethality at the end of the treatment, and the evolution of lethality with time can be related to the evolution of crosslinks; the subsequent increase could be correlated to the appearance of fragmentations. Lethality remains constant after the DL‐diepoxybutane treatment; the number of crosslinks is smaller than the number of dead phages; the disappearance of the crosslinks would compensate the biological effect of the increase of depurinated sites so that the lethality remains constant during the first hours after the end of the treatment. The inactivation of the T7 phage by any of these agents is a one‐hit process.

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