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Senescence encompasses all of the biological processes of a living organism’s approaching an advanced age (i.e., the combination of processes of deterioration which follow the period of development of an organism). The word senescence is derived from the Latin word senex, meaning “old man” or “old age” or “advanced in age”.
Cellular senescence is the phenomenon where normal diploid differentiated cells lose the ability to divide, normally after about 50 cell divisions in vitro, some cells become senescent before because of DNA double strand breaks, toxins etc. This phenomenon is also known as “replicative senescence”, the “Hayflick phenomenon”, or the Hayflick limit in honour of Dr. Leonard Hayflick who was the first to publish this information in 1965. In response to DNA damage (including shortened telomeres) cells either age or self-destruct (apoptosis, programmed cell death) if the damage cannot be repaired. In this ‘cellular suicide’, the death of one, or more, cells may benefit the organism as a whole. For example, in plants the death of the water-conducting xylem cells (tracheids and vessel elements) allows the cells to function more efficiently and so deliver water to the upper parts of a plant.
Organismal senescence is the aging of whole organisms. The term aging has become so commonly equated with senescence that the terms will be used interchangeably in this article. Aging is generally characterized by the declining ability to respond to stress, increasing homeostatic imbalance and increased risk of aging-associated diseases. Because of this, death is the ultimate consequence of aging. Differences in maximum life span among species correspond to different “rates of aging”. For example, inherited differences in the rate of aging make a mouse elderly at 3 years and a human elderly at 90 years.[citation needed] These genetic differences affect a variety of physiological processes, including the efficiency of DNA repair, antioxidant enzymes, and rates of free radical production.
Senescence of the organism gives rise to the Gompertz-Makeham law of mortality, which says that mortality rate rises rapidly with age.
Some animals, such as some reptiles and fish, age slowly. Some even exhibit “negative senescence”, in which mortality falls with age, in disagreement with the Gompertz-Makeham “law”.[1]
Whether replicative senescence (Hayflick limit) plays a causative role in organismal aging is at present an active area of investigation.
The process of senescence is complex, and may derive from a variety of different mechanisms and exist for a variety of different reasons. However, senescence is not universal, and scientific evidence suggests that cellular senescence evolved in certain species as a mechanism to prevent the onset of cancer. In a few simple species, senescence is negligible and cannot be detected. All such species have no “post-mitotic” cells; they reduce the effect of damaging free radicals by cell division and dilution. Such species are not immortal, however, as they will eventually fall prey to trauma or disease. Moreover, average lifespans can vary greatly within and between species. This suggests that both genetic and environmental factors contribute to aging.
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