This will be a blog about research dealing with the antibacterial, hexachlorophene. It will focus on hexachlorophene as a mitochondrial neurotoxin. It will cite both animal and human research that showed the toxic effects of hexachlorophene on the central nervous system myelin. It will focus on hexachlorophene's toxic effects on brain locations including the cerebellum, the hippocampus, and the brainstem.
Studies cited will include the epidemiological studies of the autopsies of babies in France who died after exposure to hexachlorophene and then showed its toxic effects in their myelin. There will also be citations of developmental effects of babies exposed to hexachlorophene. In addition to hundreds of studies about the mitochondrial neurotoxin, hexachlorophene, there have been an increasing number of recent studies of the effects of other mitochondrial neurotoxins on the central nervous system. Their effects, in many ways, reflect the common mitochondrial neurotoxic mechanism that they share with hexachlorophene.
It's especially interesting that these comparable mitochondrial neurotoxins and their effects are used as animal and human models of neurological and psychiatric disorders. These mitochondrial neurotoxins are used as models for Parkinson's, Huntington's, ALS, and other neurological disorders that affect different locations in the brain.
One of the most encouraging advancements in research is brain imaging of the effects of mitochondrial neurotoxins such as those that have become models of neurological and neuropsychiatric disorders.
In the early 1970s,when hexachlorophene was discovered to be a human mitochondrial neurotoxin, it only happened because autopsies were done after the deaths of those babies exposed to 6% hexachlorophene talcum powder. But now it is possible for hexachlorophene research to be updated. That is because its effects on those who lived can be investigated in the same way as other comparable neurotoxins have recently been reinvestigated.
Recent research on its fellow mitochondrial neurotoxins has resulted in much more information because brain imaging allows a much more sensitive exploration of the continuing toxic effects of these mitochondrial neurotoxins on the living brain. The question now is how much more we will find out when we use brain imaging to investigate what we already know is a comparatively toxic compound -- hexachlorophene.
Studies cited will include the epidemiological studies of the autopsies of babies in France who died after exposure to hexachlorophene and then showed its toxic effects in their myelin. There will also be citations of developmental effects of babies exposed to hexachlorophene. In addition to hundreds of studies about the mitochondrial neurotoxin, hexachlorophene, there have been an increasing number of recent studies of the effects of other mitochondrial neurotoxins on the central nervous system. Their effects, in many ways, reflect the common mitochondrial neurotoxic mechanism that they share with hexachlorophene.
It's especially interesting that these comparable mitochondrial neurotoxins and their effects are used as animal and human models of neurological and psychiatric disorders. These mitochondrial neurotoxins are used as models for Parkinson's, Huntington's, ALS, and other neurological disorders that affect different locations in the brain.
One of the most encouraging advancements in research is brain imaging of the effects of mitochondrial neurotoxins such as those that have become models of neurological and neuropsychiatric disorders.
In the early 1970s,when hexachlorophene was discovered to be a human mitochondrial neurotoxin, it only happened because autopsies were done after the deaths of those babies exposed to 6% hexachlorophene talcum powder. But now it is possible for hexachlorophene research to be updated. That is because its effects on those who lived can be investigated in the same way as other comparable neurotoxins have recently been reinvestigated.
Recent research on its fellow mitochondrial neurotoxins has resulted in much more information because brain imaging allows a much more sensitive exploration of the continuing toxic effects of these mitochondrial neurotoxins on the living brain. The question now is how much more we will find out when we use brain imaging to investigate what we already know is a comparatively toxic compound -- hexachlorophene.
posted by rremibgooglepages.com at 12:00 PM
1 Comments:
questions,answers,contributions,
on hexachlorophene research or on
the use of brain imaging to assess
the effects of human mitochondrial
neurotoxins? There are possibilities now to see the effect
that may have started as early as 1941 and as late as 1970s+.
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