The effect of diethanolamine on hepatic and renal phospholipid metabolism in the rat

Abstract

DEA inhibited the in vitro synthesis of both phosphatidyl choline and phosphatidyl ethanolamine in liver tissue. In each case the K 1 was approximately 3 m m DEA. DEA inhibited the formation of phosphatidyl choline competitively, and produced a mixed type of inhibition for the synthesis of phosphatidyl ethanolamine. Administration of a single dose of 250 mg/kg DEA failed to produce inhibition of synthesis, but 330 mg/kg/day caused significant inhibition when given repeatedly. The most notable reduction of choline and ethanolamine incorporation occurred in the liver. The synthesis of ethnolamine phosphoglycerides declined to 27% of the control value after 1 week of DEA administration; no further reduction was seen during the remainder of the 3-week dosing regimen. Choline incorporation fell to 82% of the control value after 1 week, and to 47% and 41% after 2 and 3 weeks of DEA administration, respectively. The incorporation of these endogenous bases in renal tissue was also decreased. Ethanolamine phosphoglyceride synthesis declined steadily throughout the dosing regimen reaching a level 41% of control. Choline incorporation declined to 71% or control by the end of the third week. The kinetics of synthesis of the phospholipid derivatives of choline, ethanolamine, and DEA proved that the former two compounds were synthesized at a faster rate and in greater quantities. They were also catabolized at a slightly faster rate than the derivatives of DEA. The biological half-life of the phospholipid derivatives of DEA is longer than that of similar derivatives of choline and ethanolamine. This may favor accumulation of the DEA-containing phospholipid during chronic exposure.