Indications of repair of radon-induced chromosome damage in human lymphocytes: an adaptive response induced by low doses of X-rays.

Abstract

Naturally occurring radon is a relatively ubiquitous environmental carcinogen to which large numbers of people can be exposed over their lifetimes. The accumulation of radon in homes, therefore, has led to a large program to determine the effects of the densely ionizing a particles that are produced when radon decays. In human lymphocytes, low doses of X-rays can decrease the number of chromatid deletions induced by subsequent high doses of clastogens. This has been attributed to the induction of a repair mechanism by the low-dose exposures. Historically, chromosome aberrations induced by radon have been considered to be relatively irreparable. The present experiments, however, show that if human peripheral blood lymphocytes are irradiated with low doses ofX-rays (2 cGy) at 48 hr of culture, before being exposed to radon at 72 hr ofculture, the yield of chromatid deletions induced by radon is decreased by a factor oftwo. Furthermore, the numbers of aberrations per cell do not follow a Poisson distribution but are overdispersed, as might be expected because high-linear energy transfer (high LET) a particles have a high relative biological effectiveness compared to low-LET radiations such as X-rays or y rays. Pretreatment with a low dose of X-rays decreases the overdispersion and leads to a greater proportion of the cells having no aberrations, or lower numbers of aberrations, than is the case in cells exposed to radon alone. It therefore appears that the putative chromosomal repair mechanism induced by low doses of sparsely ionizing radiation is also effective in reducing cytogenetic damage induced by a particles, which hitherto had been thought to be relatively immune to repair processes.

Gamma Low-Dose-Rate Ionizing Radiation Stimulates Adaptive Functional and Molecular Response in Human Aortic Endothelial Cells in a Threshold-, Dose-, and Dose Rate–Dependent Manner

“… 48 , 53 A combination of a low LET (X-rays) priming dose and a high LET (α-particles of radon gas) challenge dose leads to adaptation in human lymphocytes. 54 , 55 In cellular studies, values of priming doses and dose rates resulting in adaptive responses seem to be located within certain ranges. 46 , 51 , 56 , 57 , 58 Consequently, no adaptive response is seen with priming doses or dose rates outside this window.…”

Role of heme Oxygenase-1 in low dose Radioadaptive response

“…Evidences have suggested various possible pathways mediating RAR. For example, it was reported that the expression and transcription of some specific genes participating in DNA repair and cell cycle regulation were required for RAR in human lymphocytes [31] , [32] , [33] . It was also shown that RAR was inhibited by 3-aminobenzamide and cycloheximide and there was de novo synthesis of several proteins in response to a low-dose priming dose [34] , [35] .…”