(graying of the fur, appearance of cataract, loss of fertility). Although it should have been clear that the resemblance was onlz superficial [M3!, the hypothesis of radiation-induced aging gained momentum and stimulated much work. The interested reader might refer to the following reviews - which are only some of the many available - for more detailed evaluations of data obtained in the experimental animal [Ai, U4, C2, H3, C6, C7] and in man [Al4, AG, Fi, B6). 40. Difficulties with experimental work on aging are related to its defini- tion, to the lack of any direct measure of senescence except in term of lifespan, and to the impossibility of deciding whether pathological processes in old animals are the causes of aging, its effects or indeed aging itself. The only generalization in this respect is that in mammals the age-specific death rate increases as a function of time in a roughly exponential fashion by a constant factor for each year of the adult life, that is, that the probability of death per unit time increases with age (Figure I). However, to take this phenomenon as a measure of aging requires first the assumption that aging within each individual is paralleled by the average changes of the population where the individual belongs. In addition, there are uncertainties in sorting out, both for the individual and for the population, intrinsic and environmental factors, primary and secondary effects, specific and non-specific phenomena. ht, Tt should be pointed out that radiation is by no means the only agent producing life-shortening, but other treatments have often been reported to produce similar effects in conjunction with radiation experiments. These agents included various types of toxins and non-specific toxic substances [C8, C9] or cytotoxic drugs [C10, Ak, U6, C11, Dk] in various combinations and dosages. It appears from all these data that the effect is in general less readily induced than with radiation and that the diseases leading to precocious death are rather specific for each drug. 42, In the context of the hypothesis of radiation-induced aging, the concept has also been repeatedly discussed of differences between advanced or precocious aging on the one hand, and accelerated aging, on the other (see, for example, [C2] and [C7]). These two notions can be visualized formally in terms of the theory of radiation injury of Blair [B2, B3, BY, B5]. Actually, if one assumes that aging in an individual is determined by the sum of deleterious irreparable injuries accumulating in time; that radiation causes irreparable