Responses to Low Doses of Ionizing Radiation in Biological Systems

Abstract

Biological tissues operate through cells that act together within signaling networks. These assure coordinated cell function in the face of constant exposure to an array of potentially toxic agents, externally from the environment and endogenously from metabolism. Living tissues are indeed complex adaptive systems.To examine tissue effects specific for low-dose radiation, (1) absorbed dose in tissue is replaced by the sum of the energies deposited by each track event, or hit, in a cell-equivalent tissue micromass (1 ng) in all micromasses exposed, that is, by the mean energy delivered by all microdose hits in the exposed micromasses, with cell dose expressing the total energy per micromass from multiple microdoses; and (2) tissue effects are related to cell damage and protective cellular responses per average microdose hit from a given radiation quality for all such hits in the exposed micromasses.The probability of immediate DNA damage per low-linear-energy-transfer (LET) average micro-dose hit is extremely small, increasing over a certain dose range in proportion to the number of hits. Delayed temporary adaptive protection (AP) involves (a) induced detoxification of reactive oxygen species, (b) enhanced rate of DNA repair, (c) induced removal of damaged cells by apoptosis followed by normal cell replacement and by cell differentiation, and (d) stimulated immune response, all with corresponding changes in gene expression. These AP categories may last from less than a day to weeks and be tested by cell responses against renewed irradiation. They operate physiologically against nonradiogenic, largely endogenous DNA damage, which occurs abundantly and continually. Background radiation damage caused by rare microdose hits per micromass is many orders of magnitude less frequent. Except for apoptosis, AP increasingly fails above about 200 mGy of low-LET radiation, corresponding to about 200 microdose hits per exposed micromass. This ratio appears to exceed approximately 1 per day for protracted exposure. The balance between damage and protection favors protection at low cell doses and damage at high cell doses. Bystander effects from high-dosed cells to nonirradiated neighboring cells appear to include both damage and protection.Regarding oncogenesis, a model based on the aforementioned dual response pattern at low doses and dose rates is consistant with the nonlinear reponse data and contradicts the linear no-threshold dose-risk hypothesis for radiation-induced cancer. Indeed, a dose-cancer risk function should include both linear and nonlinear terms.

Comparison of cell repair mechanisms by means of chromosomal aberration induced by proton and gamma irradiation – preliminary results

“…It confirms our assumption in the derivation of the chisquare function that repair factor is not dependent on the dose. On the other hand, there are some indications that the repair mechanisms should work much more effectively at low doses [18], which could be investigated in future studies.…”

Cardiac computed tomography and radiation

“…Ayrıca doku kültüründe yapılan çalışmalarda çelişkiyi daha fazla arttır-maktadır. Bu çalışmalarda düşük doz radyasyonun, serbest radikalleri detoksifiye eden mekanizmaları uyarıcı etki gösterdiği saptanmıştır (21). "Radyasyon hormesisi" denen bu hipotez bugüne kadar laboratuvar ortamı dışında gösterilemese de düşük doz radyasyonun faydalı etkilerinin olabileceğini düşündü-rebilir.…”

It's Time for a New Low-Dose-Radiation Risk Assessment Paradigm—One that Acknowledges Hormesis

“…Chromosomal inversions associated with a large radiation dose were completely prevented by a subsequent small radiation dose (mild stress). Now there are many publications related to the indicated classes of radiationassociated hormesis (e.g., Liu et al 1987Liu et al , 1994Hosoi and Sakamoto 1993;Cohen 1995;Howe 1995;Khokhryakov et al 1996;Wolff 1996;Jaworowski 1997Jaworowski , 2001Rossi and Zaider 1997;Hashimoto et al 1999;Tokarskaya et al 1995Tokarskaya et al , 1997Tokarskaya et al , 2002Redpath et al 2001Redpath et al , 2003Nyström et al 2002;Wei and Sugahara 2002;Liu 2003Liu , 2004Liu , 2007Mitchel et al 2003;Pollycove and Feinendegen 2003;Sakai et al 2003;Chen et al 2004, Feinendegen et al 2004Hooker et al 2004;Ko et al 2004;Mitchel 2004Mitchel , 2005Mitchel , 2006Mitchel , 2007Scott 2004Scott , 2005aScott ,b, 2007aScott et al 2004;Zaichkina et al 2004;Elmore et al 2005;Ina and Sakai 2005;Tubiana 2005;Tubiana et al 2005;…”

“…Protective signaling intensity for protective apoptotic pathways is thought to increase with increasing numbers of genomically unstable cells (Scott 2004;, i.e., a form of natural protection. The distribution B. R. Scott of mild radiation hits among the target cell population appears also to be an important determinant of the protective signaling intensity (Bond et al 1987;Feinendegen et al 2004;Rithidech and Scott 2007), including signaling related to induced immunity (Laster et al 2007). Ullrich and Storer (1979) apparently attributed the radiation-hormesis-like observation for lung cancer in mice to systematic errors in lung cancer detection based on the methodology used.…”