Wednesday, December 14, 2005

neurochemical effect

This is another citation of hexachlorophene and other myelin toxins in a neurochemistry text.

Many chemical toxins can impair myelin formation or cause its breakdown
These include lead, cuprizone, lysolecithin, organotin, hexachlorophene and tellurium. Lead is a common environmental pollutant that causes hypomyelination and demyelination [1]. Cuprizone and lysolecithin are toxins that frequently have been used experimentally in the context of investigating remyelination [1, (image placeholder)5] (see below). Systemically administered cuprizone has a direct toxic effect on oligodendrocytes, whereas lysolecithin causes lysis of myelin sheaths themselves when administered focally. Triethyltin and hexachlorophene cause an edematous demyelination with splitting at the intraperiod line but without apparent damage to myelin-forming cells [1]. Tellurium treatment of young rats causes a highly synchronous demyelination and remyelination in sciatic nerve that is associated with the inhibition of cholesterol synthesis by some metabolite of this element [ (image placeholder)26]. A detailed description of the effects of these and other chemical toxins on the biochemistry of myelin is beyond the scope of this chapter, but they have been covered in more detail in earlier editions of this book or in other sources [1].
General undernourishment or dietary deficiencies of specific substances can lead to a preferential reduction in myelin formation
Much of the CNS myelin in mammals is formed during a relatively restricted time period of development, corresponding to the final prenatal months and the first few years of postnatal life in humans and 15 to 30 days of postnatal life in rats. Just before this rapid deposition of myelin, there is a burst of oligodendroglial proliferation. During these restricted periods of time, large portions of the metabolic activity and synthetic capacity of the brain are involved in myelinogenesis. Any metabolic insult during this "vulnerable" period may lead to a preferential reduction in myelin formation [1]. The most vulnerable period appears to be the time of oligodendroglia proliferation since animals deprived of food in this period have an irreversible deficit of myelin-forming cells and hypomyelination.

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