Chronic triethyl
tin intoxication was induced in young adult rats by oral feeding of triethyl
tin sulfate. Progressively severe
brain edema developed during the 3-month experimental period. The yield of myelin from the brains of the experimental animals decreased to almost half normal per brain, but the isolated myelin appeared morphologically normal. The analysis of whole brain showed corresponding decreases in proteolipid
protein and total
lipid, particularly
galactolipids. The proportions of the major constituents of isolated myelin (
chloroform-
methanol-insoluble residue, proteolipid
protein, and total
lipid) were unchanged despite the low yield. However, the proportion of
cholesterol increased from 16 to 21% dry weight, and that of total
galactolipid decreased from 21 to 15%, as the yield of myelin decreased. This decrease of total
galactolipid was mainly due to the decrease in cerebroside. Total
phospholipid remained constant initially but showed a slight decrease toward the end of the experiment, due mostly to decreased
ethanolamine phospholipid. There was no preferential loss or preservation of phosphatidalethanolamine. The
fatty acid composition of
sulfatide showed statistically significant shifts to less long-chain
fatty acids and less monoenoic
acids, but cerebroside and
sphingomyelin did not show significant changes in the
fatty acid composition. There was no increase in esterified
cholesterol. These findings generally support our hypothesis of nonspecific chemical abnormalities of the myelin sheath undergoing secondary degeneration. In an acute experiment, a single
intraperitoneal injection of triethyl
tin sulfate produced acute and transient
brain edema. There were slight decreases in the yield of myelin, but no detectable changes in the chemical composition.