0.5 Gy confers resistance to a subsequent high dose of γ-rays by modulating HO-1/Nrf2 and apoptosis pathways
Year: 2025
Type: article
Abstract: Ionizing radiation, from the DNA centric view, elicits biological effects and health consequences solely through energy deposition events in the cell nucleus. At higher radiation doses, this is likely true; however, at low doses, non-targeted effects, a subcategory of which is the adaptive response, tend to dominate. Controversies exist over the definition of low dose. From a radiation therapy view, it is defined as 0.5-0.7 Gy. Therefore, we investigated the effects of exposure to ionizing radiation with or without a 0.5 Gy priming dose. Techniques including comet assay, flow cytometry, fluorescence microscopy, and real-time quantitative PCR were employed. In normal lung fibroblasts (WI-38), there was a statistically significant difference in mean normalized tail moments when comparing treatment with the challenge dose alone to treatment with a 0.5 Gy priming dose prior to the challenge dose (P < 0.05). Moreover, pretreatment with a 0.5 Gy priming dose reduced G1 phase cell cycle arrest and cell death-either through apoptosis or mitotic catastrophe-induced by the subsequent 2 Gy exposure. Similarly, A549 Cells pre-exposed to a 0.5 Gy priming dose before a 2 Gy exposure showed a lower percentage of apoptosis than those exposed to the 2 Gy alone. Mechanistically, cells responded to a priming 0.5 Gy by increasing the expression of HMOX1, SOD, and Bcl2 while decreasing of IL-1β and TNF-α. In conclusion, 0.5 Gy induces an adaptive response in lung normal and cancer cell against subsequent high doses of γ-rays. Modulation of the HO-1/Nrf2 and apoptosis pathways underlie the resistance observed in primed cells.
Source: Scientific Reports
Authors: Yasser F. Ali, Ibrahim M. Hassan, Hussein M. Abdelhafez, Omar S. Desouky
Institutions: Al-Azhar University, Egyptian Atomic Energy Authority
Language: English
Subfield: Radiology, Nuclear Medicine and Imaging
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,690
Funder: Al-Azhar University
OpenAlex ID: W4408522815