Accelerated Aging: Animal Models
Experimentally Induced Models
Adult-thymectomized lab mice. When male mice are thymectomized (removal of the thymus), their mean life span is reduced, though they don't show any specific pathologies. The reduced life span is thought to be due to accelerated aging of the immune system; that is, an accelerated decline in spleen cell responsiveness to T-cell mitogens such as phytohemagglutinin and staphylococcal enterotoxin.
Dihydrotachysterol-treated rats. In laboratory tests, when young rats are given dihydrotachysterol (reduced form of tachysterol generated from irradiated ultraviolet) orally, their life span is greatly reduced. They show pathologies such as loss of body weight; atrophy of the liver, kidney, thymicolymphatic apparatus, and fat and connective tissue; generalized arteriosclerosis with calcification; and loss of elasticity of the skin. Hans Selye, et al. designated the changes induced by dihydrotachysterol a progeria-like syndrome (progeria is a condition characterized by retardation of growth, wrinkled skin, cataracts, osteoporosis, and premature senile manifestations, among other symptoms). However, cataracts are rarely observed, and osteosclerosis, not osteoporosis, occurs in the bone in dihydrotachysterol-treated rats. So, the progeria-like syndrome induced by dihydrotachysterol in rats cannot be considered an exact replica of premature senility in humans.
Radiation model. Beginning with the experiments of S. Russ and G. M. Scott, who reported an increased death rate in chronically irradiated rats, there has been repeated confirmation of the fact that sublethal total-body irradiation from an external source can increase the mortality rate or reduce the life span of mammals. In some of the experiments, the irradiated animals died prematurely with roughly the same diseases as those associated with death in the control groups. However, the diseases did not necessarily have the same incidence or order, and sometimes there were increases or decreases in the absolute incidence of certain diseases. Some diseases occurred in irradiated groups that were not observed in the control groups. A single exposure of mice to sublethal irradiation shortened life span at some doses by increasing the initial mortality rate (IMR)—the age-independent mortality rate calculated at the age of maturation—but without further accelerating the age-dependent mortality rate. The general increase of IMR without increase in the acceleration of mortality suggests that the rate of organismic senescence is not accelerated by life-shortening radiation, as discussed by Caleb E. Finch.