injuries which may add to the aging injuries; that beyond a given level of injury death of the animals occurs; that such processses within each animal may also be reflected by the Gompertz curve; then a displacement upward of this curve without change of its slope would be interpreted as precocious aging, whereas an increase of the slope would be formally equivalent to ac- celerated aging (Figure I). However, such definitions may hold formally but are difficult to be verified experimentally. 3. h3, Mechanisms of aging and life-shortening In spite of all the above important considerations of principle, attempts were often made to identify a possible effect of life-shortening with some nonspecific, diffuse, subclinical deterioration of tissues that might advance the onset of all old-age diseases to roughly the same degree. There are a great variety of non-tumorous degenerative changes to be seen in irradiated tissues [UuL, C7]. Some of these resemble superficially senescent changes, although there are profound dissimilarities between radiation~accelerated and senescent lesions W1, M3] at a closer inspection. Among the least equivocal van Cleave [V7] mentions the following: involution of the cartilage discs, involution of the thymus and all lymphatic tissues, lymphocytopenia, marrow hypoplasia, atrophy of the iris, atrophy and displasia of skin and degeneration of the skin collagen, degeneration of the elastic walls of the arteries, nephrosclerosis with glomerulosclerosis, dysplasia of the lens epithelium, vaculoization and degranulation of endocrine glands, involution of testis and ovary, generalized progressive fibrosis of the arteriocapillaries and generalized increase in fibrillar density of the interstitial connective tissue. 4h, Casarett [C7] proposed a "histopathological theory" of natural and ra- diation-induced premature aging. It rests on the notion that morphologically the most generalized deleterious change in aging mammals is an increase of the histohematic barrier - the layer of connective tissue between blood and parenchymal cells - with increase of arteriocapillary fibrosis. Functionally, a loss of selectivity of the barrier to nutrients and to wastes and a decreased efficiency of circulation would be the consequences of such changes. Under these conditions a decrease of parenchymal cells and functions would follow, with more fibrosis and loss of vasculature, in a circle becoming progessively more serious with time and leading to increased susceptibility to infection, stress, degenerative and neoplastic conditions and eventually to death.