Pre-exposure of human lymphocytes to a cGy (1 rad) of X rays halves the amount of chromosome damage induced by subsequent high dose exposures

This adaptive response to ionizing radiation, which occurs after exposures that are so low (1 cGy) that they do not induce any aberrations themselves, has been attributed to the induction of a repair mechanism that causes the restitution of X-ray-induced chromosome breaks. It has now been found that the induction occurs when cells are exposed to 1 rad in G1, S, or G2, but not G0. A period of 3-4 hours is required for full induction to occur. Furthermore, once the system has been induced, it lasts for at least 3 cell cycles. Experiments also were carried out to see if the repair mechanism induced by low dose irradiation can affect different types of clastogenic lesions induced in DNA by subsequent exposures to chemical mutagens and carcinogens. Lymphocytes were exposed to mitomycin C, a crosslinking agent, bleomycin, which induces double strand breaks in DNA, and MMS, which alkylates DNA and then leads to single strand breaks. When pre-exposed cells were challenged with high doses of bleomycin or mitomycin C, approximately half as many chromatid breaks were induced as expected. When the cells were challenged with MMS, however, approximately twice as much damage was found than was induced by MMS alone