Textbook Notes (381,222)
CA (168,408)
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HLTC22H3 (102)
Chapter 3

Chapter 3 Textbook Notes

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Department
Health Studies
Course Code
HLTC22H3
Professor
Ingrid L.Stefanovic

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HEALTH AND AGING TEXTBOOK NOTES
Chapter 3: Theories of Aging
¾ Rowe and Kahn specify that successful aging consists of good physical and mental health, as well as good
social functioning.
¾ Chaos theory shows how initially small changes can result in very large differences between systems or
individuals.
¾ Biological processes relevant to aging, we argue, fall into two categories ± those that promote homeostasis and
decelerate the aging process (such as DNA repair mechanisms and heat shock proteins) and those that amplify
the deviations and accelerate the aging process (such as free radicals)
Biological Theories of Aging
Genetic Theories
¾ The maximum lifespan of a human is about 120 years, whereas that of a fruit fly is about 30 days.
¾ In general, life spans appear to be inversely related to various factors such as metabolic rate, length of time to
maturation (especially sexual maturity), and response to stress.
Programmed Cell Death (Apoptosis)
¾ The death gene ± a gene that regulates sudden cell death, a process that is also called apoptosis.
¾ Genetic materials is not static ± different segments turn on and off, depending on the need to synthesize
proteins, perform other functions such as motility and transport, or to control the functions of other genes,
including the complicated process of cell proliferation.
¾ Apoptosis is one mechanism for the destruction of cells that have proliferated for specific purposes, such as T-
cells in the immune system, and need to be destroyed after having accomplished their task.
¾ The number of times a cell replicates may also be directly controlled by genes.
Stochastic Processes
¾ Aging may be a function of random (or stochastic) errors.
¾ Replication error is one of the leading theories of aging.
¾ DNA is susceptible to damage by a host of environmental factors, including a variety of chemical agents.
¾ 'DPDJHWR'1$FDQLPSDLUDFHOO¶VDELOLW\WRV\QWKHVL]HSURWHLQVDQGRWKHUVXEVWDQFHVDQGRUUHVSRQGWR
regulation.
¾ Cells can limit damage by turning off the damage segment and turning on identical backup segments by using
DNA repair mechanisms to correct the error.
¾ Eventually, however, the cell runs out of backups, and it can no longer function adequately.
DNA Repair Mechanisms
¾ Many different factors can damage DNA, including light, ultraviolet and other types of radiation, exposure to
toxic chemicals, and the oxidation process itself.
¾ There are several mechanisms of DNA repair. The primary ones include base excision repair, nucleotide
excision repair, mismatch repair, and repair of strand breaks.
¾ If an error is caught, replication is stopped so that repairs can be made.
¾ If the error burden is too severe, the cell undergoes apoptosis.
Molecular/Cellular Theories of Aging
Oxidation
¾ One of the most popular theories of aging is the free radical theory.
¾ Free radicals or reactive oxygen species (ROS) are molecules that are generated during the oxidation process in
cells.
¾ Each ROS has an unpaired electron; thus, they are unstable and extremely chemically reactive. They can
interfere with the functions of other molecules in the cell, including DNA replication, the metabolism of fatty
acid chains, proteins synthesis.
¾ In part, free radicals such as superoxide can damage proteins by causing them to unfold; without proper
structure, proteins cannot perform their function correctly.
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HEALTH AND AGING TEXTBOOK NOTES
¾ Sohal and Weindruch (1996) argue that the concentration of free radicals (and thus cell damage) increase with
age, because (a) more free radicals are generated in aging cells, (b) there appears to be a decrease in the ability
of the cell to generate antioxidants, and (c) cellular mechanisms become less efficient.
Lipofuscin
¾ Aging cells also accumulate waste matter called lipofuscin, a dark mixture of lipoproteins and various waste
products.
¾ Lipofuscin is found in nearly all cell types, from heart muscle cells to neurons, and increases with age.
¾ One recent finding suggests that there may be different types of lipofuscin, one on which may be associated
ZLWK$O]KHLPHUVGLVHDVH
¾ Accumulation of lipofuscin may be a biomarker for metabolic rate, because it reflects oxidation and thus the
production of free radicals.
Heat Shock Proteins
¾ There are many different types of cellular repair mechanisms, which can be considered aging decelerators. The
most important of these for the aging process may be heat shock proteins (Hsps).
¾ They play a major role in protecting cells from nearly every kind of stressor, from radiation to infection to
oxidation.
¾ In addition to protecting cells against the effects of stress, they also are important in promoting healthy cell
growth and proliferation.
¾ Small Hsps protect cells from stress oxidative processes by regulating enzymatic processes necessary for repair
and apoptosis.
¾ They also play a major role in the inflammatory process.
¾ Hsps are one of the mechanisms that control inflammation. If they cannot repair a cell, they may help the cell to
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¾ In apoptosis, a cell systematically dismantles and repackages itself and is readily reabsorbed by the surrounding
cells. But in necrosis, the cell ruptures spewing toxic chemicals and distress signals, leading to an increase in
the inflammatory process.
¾ Thus, Hsps may aid in the healing process by dismantling damage cells, or they may contribute to chronic
inflammation.
Homeostasis
¾ To function, organisms must maintain a certain level of homeostasis, that is, stability in intra- and extracellular
environmental conditions, such as pH balance, blood pressure, heart rate, temperature, and electrolyte and fluid
balance.
¾ Homeostasis requires communication among the various organ systems and is largely regulated by the
autonomic nervous system via the neuroendocrine system.
¾ There is good evidence to suggest that as we age, it becomes harder to maintain homeostasis.
¾ Problems in homeostasis regulation may be due to one of three factors:
1) There may be a decline in the production of hormones or other type of regulatory peptides. Ovarian
decrease in estrogen production is a good example of this.
2) The target organs may become less responsive, due either to fewer receptors for neuroendocrine
signals or to degradation in the functioning of receptor sites on cell surfaces.
3) The target organ may synthesize less than optimal amounts of its product, due either to fewer secretory
cells or less efficient production.
¾ A number of illnesses commonly associated with aging reflect these problems in homeostasis, such as
orthostatic hypertension and diabetes.
Wear-and-Tear Theories
¾ One of the earliest theories of aging was the simple wear-and-tear theory ± that is, with continual use, our
organs and joints simply wear out.
¾ For most organ systems, this early theory does not hold.
¾ The one exception to this adage appears to be skeletal joints. One of the causes of osteoarthritis is wear and tear
on the joints, and it is nearly universal in late life.
¾ However, it is also true that total bed rest in the elderly can result in stiffened, immobile joints (contracture), as
well as problems with a host of other systems.
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Description
HEALTH AND AGING TEXTBOOK NOTES Chapter 3: Theories of Aging Rowe and Kahn specify that successful aging consists of good physical and mental health, as well as good social functioning. Chaos theory shows how initially small changes can result in very large differences between systems or individuals. Biological processes relevant to aging, we argue, fall into two categories those that promote homeostasis and decelerate the aging process (such as DNA repair mechanisms and heat shock proteins) and those that amplify the deviations and accelerate the aging process (such as free radicals) Biological Theories of Aging Genetic Theories The maximum lifespan of a human is about 120 years, whereas that of a fruit fly is about 30 days. In general, life spans appear to be inversely related to various factors such as metabolic rate, length of time to maturation (especially sexual maturity), and response to stress. Programmed Cell Death (Apoptosis) The death gene a gene that regulates sudden cell death, a process that is also called apoptosis. Genetic materials is not static different segments turn on and off, depending on the need to synthesize proteins, perform other functions such as motility and transport, or to control the functions of other genes, including the complicated process of cell proliferation. Apoptosis is one mechanism for the destruction of cells that have proliferated for specific purposes, such as T- cells in the immune system, and need to be destroyed after having accomplished their task. The number of times a cell replicates may also be directly controlled by genes. Stochastic Processes Aging may be a function of random (or stochastic) errors. Replication error is one of the leading theories of aging. DNA is susceptible to damage by a host of environmental factors, including a variety of chemical agents. ,2,J094.,3L25,L7,.0OO8,-LOL994839K08L]057490L38,349K078:-89,3.08,3 4770854394 regulation. Cells can limit damage by turning off the damage segment and turning on identical backup segments by using DNA repair mechanisms to correct the error. Eventually, however, the cell runs out of backups, and it can no longer function adequately. DNA Repair Mechanisms Many different factors can damage DNA, including light, ultraviolet and other types of radiation, exposure to toxic chemicals, and the oxidation process itself. There are several mechanisms of DNA repair. The primary ones include base excision repair, nucleotide excision repair, mismatch repair, and repair of strand breaks. If an error is caught, replication is stopped so that repairs can be made. If the error burden is too severe, the cell undergoes apoptosis. MolecularCellular Theories of Aging Oxidation One of the most popular theories of aging is the free radical theory. Free radicals or reactive oxygen species (ROS) are molecules that are generated during the oxidation process in cells. Each ROS has an unpaired electron; thus, they are unstable and extremely chemically reactive. They can interfere with the functions of other molecules in the cell, including DNA replication, the metabolism of fatty acid chains, proteins synthesis. In part, free radicals such as superoxide can damage proteins by causing them to unfold; without proper structure, proteins cannot perform their function correctly. www.notesolution.com
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