| Abstract: | 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. |
