EFFECT OF DIETHANOLAMINE ON HEPATIC AND RENAL PHOSPHOLIPID-METABOLISM IN THE RAT

DEA inhibited the in vitro synthesis of both phosphatidyl choline and phosphatidyl ethanolamine in liver tissue. In each case the K1 was approximately 3 mm 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. © 1979.