Abstract
X-rays (XR) are electromagnetic waves capable of inducing significant biological effects in living organisms. Although widely used in medicine and industry, the impact of low-dose XR exposure on human health remains insufficiently characterized. XR can generate direct and indirect DNA damage such as single- and double-strand breaks, base modifications, and DNA-protein crosslinks, leading to chromosomal alterations that disrupt cellular homeostasis and may contribute to disease development. Although previous studies have reported general increases in cytogenetic damage at low exposures, they seldom provide detailed descriptions of which chromosomes are most affected, which structural or numerical alterations predominate, or how frequently each alteration occurs. This study aimed to characterize the type and frequency of chromosomal alterations and the spectrum of genetic damage, including both clonal and non-clonal alterations, in human lymphocytes exposed in vitro to a low X-ray dose (94.33 mGy), using non-exposed samples as controls. Peripheral blood was collected from 12 healthy donors, and genetic damage was assessed using GTG-banding cytogenetics and the cytokinesis-block micronucleus assay. Irradiated samples exhibited a significantly higher frequency of chromosomal alterations and fragile sites compared with their respective controls (p ≤ 0.0093). Among numerical alterations, monosomies were the most frequent, with chromosomes 8 and 21 being the most commonly affected, detected in 50% of irradiated samples. Structural chromosomal alterations predominantly involved chromosomes 11, 16, and 17, while recurrent deletions included del(15)(q22) and del(16)(q12). Among heterochromatic variants, chtb(9)(q12) was the most frequent, and fra(9)(q12) represented the most prevalent fragile site. MN frequency increased significantly after irradiation (p = 0.0214), and women exhibited higher MN frequencies than men regardless of treatment (p = 0.0224). Overall, these findings indicate that low-dose XR exposure is associated with detectable chromosomal damage and underscore the relevance of biosafety practices and cytogenetic monitoring approaches in contexts involving XR exposure, even at doses traditionally considered safe.