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Stress‐Induced Premature Senescence: Essence of Life, Evolution, Stress, and Aging

The stress syndrome was discovered accidentally by Hans Selye while searching for new hormones in the placenta.1 After injecting rats with crude preparations, Selye found adrenal enlargements and involution of thymus and lymph nodes, which he thought were specific for a particular hormone. It occurred to Selye that these symptoms might represent a nonspecific response to noxious agents. Indeed, this was found to be the case when he injected rats with diverse agents. Selye defined the stress response as the “general adaptation syndrome.”2,3 According to this theory, the initial reaction to stress is shock, it is followed by a countershock phase, and gradually resistance develops to the stressor. This resistance may turn into exhaustion, however, if the stressor persists, and death may ensue. Both specific and nonspecific resistance develops during stress.4 In his last scientific book, Selye defined biologic stress as “the non-specific response of the body to any demand made upon it.”5 Beside the transfer of the word “stress” from physics to biology, Selye also coined the words corticosteroids, glucocorticoids, and mineralocorticoids.6 Nowadays, the concept of stress has invaded most fields of the biologic, medical, and social sciences. Cellular and molecular biology has become interested in the study of the stress response of human, animal, and plant cells, the consensus being that “any environmental factor potentially unfavourable to living organism” is stress.7 It is also generally agreed that “if the limits of tolerance are exceeded and the adaptive capacity is over-worked, the result may be permanent damage or even death.”8 Three phases of the stress response have been defined based on experimental observations: (1) the response phase of alarm reaction with deviation of functional norm, decline of vitality, and excess of catabolic processes over anabolism, (2) the restitution phase or stage of resistance with adaptation processes and repair processes, and (3) either the end phase, that stage of exhaustion or long-term response when stress intensity is too high, leading to overcharge of the adaptation capacity, damage, chronic dis-