Adaptive response of human lymphocytes to low-level radiation from radioisotopes or X-rays

Effect of 3-aminobenzamide on chromosome damage in human blood lymphocytes adapted to bleomycin

“…The radiation dose used for adaptation seemed to have an effect; so also the time-interval between the adaptation and challenge doses (Shadley etal., 1987), the dose rate and the quality of radiation (Wiencke et al, 1987). Sankaranarayanan et al (1989) have confirmed the original results of Olivieri et al (1984). More recently, Wolff et al (1988) reported that human blood lymphocytes adapted to low doses of ionizing radiation became refractory to chromosome damage, not only by a high dose of radiation but also by chemical mutagens that induce similar kinds of lesions in DNA.…”

The Influence of Individual Genome Sensitivity in DNA Damage Repair Assessment in Chronic Professional Exposure to Low Doses of Ionizing Radiation

“…When the unrepaired amount of damage was compared, the results are implicating the existence of adaptive response in professionally exposed individuals to low doses of ionising radiation. Adaptive response in human lymphocytes has been described by other authors (Olivieri & Bosi, 1990;Sankaranarayanan et al, 1989;Shadley &Wolff, 1987;Wiencke et al, 1986;Wolff et al, 1990;Wolff, 1992Wolff, , 1996. Aka et al (2004) reported the existence of residual damage in tail intensity 60 and 120 minutes after the exposure to dose of 2 Gy.…”

“…Although former results showed the existence of radio adaptive response, our results did not confirm the relationship between primary DNA damage and adaptive response. Few authors have also shown lower DNA damage levels after the repeated exposure to ionising radiation (Sankaranarayanan et al, 1989;Wang et al, 1991;Ikushima, 1992;Domingues et al, 1993). APE1 gene is involved in BER repair.…”

An Examination of Radiation Hormesis Mechanisms Using a Multistage Carcinogenesis Model

“…This adaptive response to IR, which occurs after exposures that are so low (0.005-0.01 Gy) that they do not induce discernible aberrations themselves, has been attributed to the induction of a repair mechanism that causes the restitution of X-rayinduced chromosome breaks (Wolff, 1998). Variations and the absence of adaptive responses have also been reported (Jacobson-Kram and Williams, 1988;Bauchinger et al, 1989;Bosi and Olivieri, 1989;Sankaranarayanan et al, 1989;Schmid et al, 1989;Hain et al, 1992;Müller et al, 1992;Wojcik et al, 1992Wojcik et al, , 1993Shadley, 1994;UNSCEAR, 1994;Vijayalaxmi et al, 1995;Boothman et al, 1996;Raaphorst and Boyden, 1999;Sorensen et al, 2002). Azzam et al (1996) exposed quiescent mouse fibroblasts (C3H 10T1/2) cells to doses of 1-100 mGy -rays and observed that the risk of neoplastic transformation was reduced from the spontaneous level to a rate three-to four-fold below that level.…”