The pathogenesis of hexachlorophene neuropathy: in vivo and in vitro studies

In rats fed hexachlorophene (HCP), hindlimb weakness developed within 2 to 3 wk and sciatic nerves showed widespread myelin intraperiod line splitting, intramyelinic vacuolization and occasional segmental demyelination. Myelin was prepared from the nerves of the hexachlorophene treated rats; in comparison to controls, the myelin yield was reduced by about 40%. Hexachlorophene also caused myelin disruption in vitro; when rat cerebellum tissue cultures were exposed to hexachlorophene, myelinic blebs appeared within 12 hr. When chick embryo sciatic nerves were incubated with [¹⁴C]HCP, the hexachlorophene was rapidly bound to the nerves; binding was solely by hydrophobic interaction and was not myelin specific. After a latent period of 1 hr hexachlorophene caused a profound inhibition of protein and lipid synthesis by the chick nerves. During incubation with hexachlorophene, nerve content of adenosine triphosphate fell, with consequent diminution in the rate of activation of sulfate to 3' phosphoadenosine 5' phosphosulfate.