triethyltin and Demyelinating-Diseases

Oligodendrocytes establish relationships with axons at myelination which commit the cell to make and then maintain certain volumes of myelin. As a result of this oligodendrocytes are a heterogenous population of cells. At one extreme, large cells support a single internode on large diameter axons while at the other, small cells support many internodes on small diameter axons. Although it is common practice to separate chemicals which cause vacuolation of myelin sheaths from those which bring about cell death and thus demyelination, many compounds produce vacuolation and/or cell degeneration depending on concentration; an observation which suggests that myelin sheath-associated vacuolation reflects oligodendrocyte toxicity rather than a specific myelinopathy. The restoration of myelin sheath-axon relationships following chemically induced demyelination requires a complex sequence of cell-cell interactions to occur in an orderly manner if new myelin sheaths are to be formed. Recruitment of new oligodendrocytes can be separated from the interaction of oligodendrocytes with axons which results in the laying down of a myelin sheath. The latter event can only take place in the absence of demyelinating agents and in the presence of astrocytes.

Topics: 6-Aminonicotinamide; Animals; Axons; Cuprizone; Demyelinating Diseases; Ethidium; Isoniazid; Mice; Myelin Sheath; Neuroglia; Oligodendroglia; Rats; Triethyltin Compounds

The toxicology of tin is almost entirely the toxicology of the organic compounds of tin, for the metal itself and its inorganic compounds appear to be nearly harmless for practical purposes. Furthermore, the neurotoxicity of organotin is essentially that of trimethyltin and triethyltin.

Topics: Animals; Bile Duct Diseases; Chemical and Drug Induced Liver Injury; Demyelinating Diseases; Guinea Pigs; Humans; Immunity, Cellular; Immunologic Deficiency Syndromes; Mice; Nervous System Diseases; Organotin Compounds; Rats; Species Specificity; Tin; Triethyltin Compounds; Trimethyltin Compounds

The question of what happens to cholesterol in the adult central nervous system during its slow turnover has been addressed using rats with brain and spinal cord labeled with [4-14C]cholesterol upon intracerebral injection of labeled cholesterol into rats at 10-12 days of age. At six months after injection, 14C was found only in the brain and spinal cord and was slowly released via the rat's urine. When labeled rats were given demyelinating agents (triethyl tin chloride, hexachlorophene, sodium cyanide) and when experimental allergic encephalomyelitis was induced, a measurable increase in urinary 14C label above control levels was found. It was concluded that there is a direct relationship between the experimental demyelination induced and the increased release of cholesterol metabolites into urine. The study suggests that a clinical method could be developed to determine the rate of central nervous system demyelination by measuring the amount of urinary cholesterol metabolites.

Topics: Animals; Carbon Radioisotopes; Central Nervous System Diseases; Cholesterol; Demyelinating Diseases; Disease Models, Animal; Encephalomyelitis, Autoimmune, Experimental; Hexachlorophene; Rats; Rats, Inbred Lew; Rats, Sprague-Dawley; Sodium Cyanide; Starvation; Triethyltin Compounds