A major component of the radiation effect: interference with endocellular control of cell proliferation and differentiation.
Cytological investigations with diploid and autotetraploid plant materials reveal that cytoplasmic growth, including the propagation of autoreduplicating cytoplasmic units such as mitochondria and proplastids, continues during the radiation-induced mitotic delay, thus increasing the ratio of cytoplasmic amount: nuclear ploidy. In accordance with a control mechanism, detected in the plant endosperm, this increase causes mitotic inhibition due to any early induction of otherwise normal differentiation processes. Although mutations are not a prerequisite, they can act in an auxiliary manner by quantitative action. The contribution of 'early differentiation' to non-survival varies according to irradiation conditions and can outweigh the direct effects of irreversible genetic damage. Therefore, a higher level of ploidy cannot improve survival significantly, if mitotically-active tissues are irradiated under the usual conditions. Corresponding observations are known from animals. The results suggest that the control mechanism of the endosperm is (a) general to multicellular organisms, and (b) can be modulated by extracellular agents.
D002454:Cell Differentiation / Q000528:radiation effects; D002455:Cell Division / Q000528:radiation effects; D002467:Cell Nucleus / Q000032:analysis; D002470:Cell Survival; D002869:Chromosome Aberrations; D003593:Cytoplasm / Q000528:radiation effects; D004247:DNA / Q000032:analysis; D004171:Diploidy; D004307:Dose-Response Relationship, Radiation; D008938:Mitosis / Q000528:radiation effects; D010944:Plants / Q000528:radiation effects*; D011123:Polyploidy; D011830:Radiation Effects; D014965:X-Rays
D004247:DNA