Adaptive responses to low doses of radiation or chemicals: their cellular and molecular mechanisms

• Published in: Cellular and molecular life sciences : CMLS 2019-04, Vol.76 (7), p.1255-1273
• Main Authors: Guéguen, Yann, Bontemps, Alice, Ebrahimian, Teni G.
• Format: Article
• Language: English
• Subjects: Antioxidants; Antioxidants - metabolism; Apoptosis; Autophagy; Autophagy - drug effects; Autophagy - radiation effects; Biochemistry; Biological effects; Biomedical and Life Sciences; Biomedicine; Cancer; Cell Biology; Cell cycle; Cell death; Cell survival; Cellular stress response; Deoxyribonucleic acid; DNA; DNA damage; DNA repair; DNA Repair - drug effects; DNA Repair - radiation effects; Environmental Pollutants - chemistry; Environmental Pollutants - toxicity; Health risks; Humans; Inflammation; Inflammatory response; Ionizing radiation; Life Sciences; Mitogen-Activated Protein Kinases - metabolism; Molecular modelling; NF-E2-Related Factor 2 - metabolism; NF-κB protein; Occupational exposure; Occupational health; Organic chemistry; p53 Protein; Phagocytosis; Protein folding; Proteins; Radiation dosage; Radiation protection; Radiation standards; Radiation, Ionizing; Review; Risk factors; Signal Transduction - drug effects; Signal Transduction - radiation effects; Unfolded Protein Response - drug effects; Unfolded Protein Response - radiation effects
• ISSN: 1420-682X; 1420-9071
• DOI: 10.1007/s00018-018-2987-5

This article reviews the current knowledge on the mechanisms of adaptive response to low doses of ionizing radiation or chemical exposure. A better knowledge of these mechanisms is needed to improve our understanding of health risks at low levels of environmental or occupational exposure and their involvement in cancer or non-cancer diseases. This response is orchestrated through a multifaceted cellular program involving the concerted action of diverse stress response pathways. These evolutionary highly conserved defense mechanisms determine the cellular response to chemical and physical aggression. They include DNA damage repair (p53, ATM, PARP pathways), antioxidant response (Nrf2 pathway), immune/inflammatory response (NF-κB pathway), cell survival/death pathway (apoptosis), endoplasmic response to stress (UPR response), and other cytoprotective processes including autophagy, cell cycle regulation, and the unfolded protein response. The coordinated action of these processes induced by low-dose radiation or chemicals produces biological effects that are currently estimated with the linear non-threshold model. These effects are controversial. They are difficult to detect because of their low magnitude, the scarcity of events in humans, and the difficulty of corroborating associations over the long term. Improving our understanding of these biological consequences should help humans and their environment by enabling better risk estimates, the revision of radiation protection standards, and possible therapeutic advances.