Effects of Mitochond
Effects of Mitochondrial Toxins Including Hexachlorophene : The Process of Liver Damage
Other papers have reviewed the effects of hexachlorophene as a mitochondrial neurotoxin. This paper will review an additional effect of hexachlorophene and other toxins of its preventing the mitochondrial production of ATP.
Adenosine Triphosphate (ATP) is vital because it is used to store energy in the cell's mitochondria. During oxidative stress this stored energy is used to defend the cell fom damage or death.
The specific result of these mitochondrial toxins on the liver is damage or death to the liver cells. In addition to hexachlorophene there are a number of herbicides and pesticides that affect the mitochondria of liver cells and, in turn, affect the viability of these cells. One of these herbicides is called dinoseb. Liver cell death by dinoseb starts in the mitochondria because it also leads to the depletion of ATP.
Another mitochondrial toxin to the liver is called Tacrine. It has been used in the treatment of Alzheimer's disease. However tacrine has been shown to accumulate within the mitochondria, and has targeted the mitochondrial DNA. Again, its effect of uncoupling oxidative phosphorylation is ATP depletion.
So,hexachlorophene, in addition to its neurological effects, is also toxic to liver cells. Again, hexachlorophene is a mitochondrial liver toxin as well as a neurotoxin. In both the brain and the liver it uncouples oxidative phosphorylation and interferes with the production of ATP. There is this same biochemical mechanism with similar effects. This depletion can result in either cellular damage or death. Repeated use of hexachlorophene repeats these toxic cellular effects.
Other papers have reviewed the effects of hexachlorophene as a mitochondrial neurotoxin. This paper will review an additional effect of hexachlorophene and other toxins of its preventing the mitochondrial production of ATP.
Adenosine Triphosphate (ATP) is vital because it is used to store energy in the cell's mitochondria. During oxidative stress this stored energy is used to defend the cell fom damage or death.
The specific result of these mitochondrial toxins on the liver is damage or death to the liver cells. In addition to hexachlorophene there are a number of herbicides and pesticides that affect the mitochondria of liver cells and, in turn, affect the viability of these cells. One of these herbicides is called dinoseb. Liver cell death by dinoseb starts in the mitochondria because it also leads to the depletion of ATP.
Another mitochondrial toxin to the liver is called Tacrine. It has been used in the treatment of Alzheimer's disease. However tacrine has been shown to accumulate within the mitochondria, and has targeted the mitochondrial DNA. Again, its effect of uncoupling oxidative phosphorylation is ATP depletion.
So,hexachlorophene, in addition to its neurological effects, is also toxic to liver cells. Again, hexachlorophene is a mitochondrial liver toxin as well as a neurotoxin. In both the brain and the liver it uncouples oxidative phosphorylation and interferes with the production of ATP. There is this same biochemical mechanism with similar effects. This depletion can result in either cellular damage or death. Repeated use of hexachlorophene repeats these toxic cellular effects.
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