Vertebrate Radiobiology: Histopathology and Carcinogenesis

Abstract

Knowledge of the histopathologic and carcinogenic effects of ionizing radiation has been amplified greatly under the impetus of atomic fission. Recent research has yielded significant contributions on relationships be­ tween dose, dose rate, type of radiation (electromagnetic and particulate) , and biologic effectiveness; on synergistic and antagonistic factors modifying the biologic effectiveness of radiation; on radiation protection ; on the mechanisms of direct and indirect effects resulting in acute and delayed radiation injury, notably hemorrhage, microbic invasion, leukemia, neo­ plasia, and cataract; and on species and strain differences in radiosensitivity. T he older literature is reviewed by Lacassagne (1 , 2, 3) and Warren et al. (4, 5). Bloom (6) describes in detail the histologic studies of the Plutonium Project, and Hempelmann et al. (7, 8) survey radiation effects in man. Relevant references are included in recent reviews by Brues (9) , Cronkite & Brecher (10) , Curtis ( 1 1) , and Patt (12) , and the carcinogenic action of radiations has been discussed in historical perspective by Furth & Lorenz (13) . It i s accepted that particulate irradiation produces essentially the same changes as electromagnetic irradiation: both act ultimately by causing ioniza­ tions and may be compared quantitatively by expressing ionization values in terms of rep and rem [Evans (14)]. In general, adult and resting . cells are radioresistant, while mitotic or metabolically active cells are sensi­ tive: thus, susceptibility to acute injury is a function of cellular replacement or growth. Liability to tumor-induction, on the contrary, is not dependent on mitotic activity alone: e.g., the replacement rate of epithelial cells of the cornea and small intestine is high, yet they do not give rise to tumors. It seems that both direct and indirect mechanisms are at play in determining the magnitude and character of radiation damage, particularly with respect to induction of neoplasia, but knowledge of these mechanisms is still scant.