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NON GENETIC CELLULAR THEORY OF AGING

WASTE ACCUMULATION THEORY


Also known as Accumulative Waste Theory of Aging and Garbage Accumulation Theory of Aging In the course of a cells life spans they produce more waste than they can properly eliminate. This waste can include various toxins which when accumulated to a certain level, can interfere with normal cell function, ultimately killing the cell. Damaged molecules by oxidation and their byproducts (also damaged mitochondria), accumulate in post mitotic cells which causes: Dysfunction AGING -Toxicity - CELL DEATH

Asserts that aging results from the accumulation of harmful substances in the cell of an organism a kind of cellular constipation results if cells accumulate more waste than can be disposed of efficiently. HOW DOES ACCUMULATION AFFECT THE CELL? The cells structural organization is changed The cellular components are displaced, thereby impeding cellular and metabolic function Causing damage to cells secondary to toxicity WHERE DOES WASTE ACCUMULATION DEVELOP? Cardiac cells Skeletal cells Nerve Cells or Neurons WHY DOES ACCUMULATION HAPPEN? Due to lack of turnover The actively dividing cells are capable of diluting the amount of damage during cell division EXPERIMENTAL BASIS

Lipofuscin accumulation Lipofuscin is formed by a complex reaction that binds fat in the cells to proteins. This waste accumulates in the cells as small granules and increases in size as a person ages. Builds up as a person ages This Cellular Garbage interferes with cellular functioning because it takes up space and serves no useful purpose. This may ultimately result in the death of the cell.

DEPRIVATION THEORY
aging is caused by vascular changes that deprives cells of essential nutrients and oxygen Purposes that oxygen deprivation leads to senescence of deprived cells. EFFECT OF VASCULAR CHANGES Oxygen Deprivation Hypoxia, or oxygen deciency, interferes with aerobic oxidative respiration and is an extremely important and common cause of cell injury and death. Nutritional Imbalances remain a major cause of cell injury or senescence

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