Notwithstanding the above, the spectre of radioactive leaks originating from the reiterated Russian bombings over the nuclear site of Zaporizhzhia (Ukraine), along with those deriving from the recent bombings made by the Israel and the USA airforces on Iran's highly enriched uranium plants, looms again over the whole mankind.
While the biological effects appear to be similar in people as well as in terrestrial and aquatic mammals exposed to both ionizing (such as alfa, beta, gamma particles and X-rays) and non-ionizing (such as UV-rays) radiations, acute and/or chronic damages are commonly reported to occur.
The former ones are comparable to heat-related/associated biological effects, with more or less severe and extensive burns developing in relation to the duration of exposure alongside the distance from the radiation source (1).
Conversely, the far more alarming chronic effects refer to the biochemical damage inflicted on cellular macromolecules like membrane lipids (undergoing rapidly expanding peroxidation phenomena), proteins (both enzymatic and non-enzymatic), sugars and, above all, nucleic acids (DNA and RNA), with the latter ones suffering from widespread degradation/denaturation/rupture processes, accompanied by genomic mutations culminating in irreversible changes (1). Among the over 200 cell populations inhabiting our bodies alongside those of terrestrial and aquatic mammals, highly variable degrees of susceptibility to radiation have been reported, with "labile" - alias intensely replicating - cells (male and female gametocytes, bone marrow stem cells, basal layer epidermis cells, etc.) exhibiting the highest sensitivities, as clearly shown by subsequent "aplasia/hypoplasia" and/or tumour development (2,3).
Up to a "given magnitude" of damage, there are a number of molecular players acting in concert to revert the cellular alterations, thus preventing further negative effects. Within such a dynamic context, a key actor is represented by p53 - alias the "cell guardian" -, a transcription factor produced by a gene located on chromosome 17 in human cells. More in detail, p53 intervenes either in DNA repair or, alternatively, leading to cellular apoptosis - alias "programmed cell death" - when consistent genetic damages are underway. Unfortunately, also the p53-encoding gene is not spared by radiation-induced mutations. As a consequence, rather than orchestrating the establishment of an apoptotic "cascade", mutated p53 will behave like an early "biochemical signature" of a progressive "genetic instability" process, thereby driving cells towards a neoplastic growth (1-3).
As a concluding remark, I believe that, based upon the evident lack of geographic boundaries clearly highlighted, once again, by the nuclear accidents of Chernobyl and Fukushima, a multidisciplinary, holistic and "One Health"-inspired approach would be absolutely needed in handling, counteracting and preventing future nuclear accidents, all the more in the light of the scary war theatres in Ukraine and Iran.
Historia magistra vitae!
References
1) Altucci L, Berton G, Stivala LA, Moncharmont B. (2019). Patologia Generale, Volume 1, Idelson-Gnocchi Editore, Naples, Italy.
2) Honjo Y, Ichinohe T. (2025). Neural crest cells are sensitive to radiation-induced DNA damage. Tissue Cell 94:102774.
DOI: 10.1016/j.tice.2025.102774.
3) Lopes R, Teles P, Santos J. (2025). A systematic review on the occupational health impacts of ionising radiation exposure among healthcare professionals. J. Radiol. Prot. 45(2).
DOI: 10.1088/1361-6498/added2.