Essay, Research Paper Mitochondria are the powerhouse of the cell. Their sole responsibility is to provide energy for the cell. They do this by synthesizing a molecule known as ATP, which the cell uses as energy. Mitochondria are different from the rest of the cell organelles because they contain their own DNA outside the nucleus.
Essay, Research Paper
Mitochondria are the powerhouse of the cell. Their sole responsibility is to provide energy for the cell. They do this by synthesizing a molecule known as ATP, which the cell uses as energy. Mitochondria are different from the rest of the cell organelles because they contain their own DNA outside the nucleus.
Mutations in this DNA have been found to be linked to Alzheimer s and other neurodegenerative diseases. Mutations in the DNA cause the mitochondria to function in other ways than it usually does. Generally these mutations cause the mitochondria to produce ATP less efficiently. Nuclear DNA is a lot less prone to these mutations because it has things that check and fix problems when they occur.
Mutations are passed from cell to cell randomly. When a cell divides it can pass both normal mitochondria and mutated ones in any ratio to the two daughter cells. These mutations can only be inherited through your mother since she is the one that provides all the mitochondria at conception.
In the process of making ATP oxygen free radicals are produced. These free radicals are very harmful and destructive causing breakdowns in mitochondria and more mutations in its DNA. The mutations are believed to produce free oxygen radicals. Mitochondria after long periods of time are able to produce less and less amounts ATP because of the free radicals deteriorating them. This for most of the cells is usually not that much of a problem because cells make excess ATP. But in mutated cells that are big ATP consumers, like brain and muscle cells, these cells can sometimes lack enough ATP to function and die because of it.
Work was done at the University of California, San Francisco to prove that oxygen radicals breakdown mitochondria. They used mice that lacked an enzyme (Manganese superoxide dismutase) that neutralizes free radicals during oxygen metabolism. The mice died within 10 days and samples taken of mitochondria from the heart tissue of the mice revealed the mice died because of problems with the mitochondria.
The death of brain cells is what is leading scientists to believe is one of the causes of Alzheimer s disease along with other neurodegenerative diseases. Scientist took brain tissue samples of people who died with the disease and found that over five percent of them had genetically mutated mitochondria DNA, this percentage would have been under one percent if it had been taken from people randomly without the disease.
As people grow older they usually feel like they have less and less energy to do things. This feeling of tiredness in older people can be attributed the less and less amounts of ATP being able to be produced by the mitochondria. Heart Attacks that people attribute to old age can sometimes be caused by the muscle cell in the heart not having enough energy to function correctly.
Diabetes Mellitus is another mitochondria related disease. Type II, mature onset diabetes is rooted in inherited mitochondria DNA defects still to be discovered. Research has already discovered that known mitochondria DNA rearrangement and base substitution mutations can at times cause Type II diabetes.
In conclusion, mitochondria research can hold the clues for curing some of the most devastating old age diseases.
1) Finkel, Elizabeth. Piecing together the puzzle of aging , The Lancet, Oct 18, 1997 v350 n9085 p1150.
2) Travis, John. Do brain cells run out of gas? , Science News, August 5, 1995 v148 n6 p84.
3) Stepenson, Joan. A role for mitochondria in age-related disorders? , JAMA, The Journal of the American Medical Association, May 22,1996 v275 n20 p1531(2).
4) Fackelmann, Kathleen. Power failure: what happens when muscle cells run out of fuel , Science News, Sep 27, 1997 v152 n13 p206(2).
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