2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a highly toxic environment
al contaminant, interferes with retinoid homeostasis. To elucidate the
underlying mechanism, the activities of lecithin:retinol and acyl-CoA
:retinol acyltransferase (LRAT and ARAT) were determined in liver, kid
ney, and hepatic parenchymal and nonparenchymal cell fractions from ra
ts 7 days after a single oral dose of 10 mu g TCDD/kg body weight(b.w)
. Severely depressed LRAT activity in hepatic stellate cells, and grea
tly increased LRAT activity in kidneys, as well as decreased ARAT acti
vity in stellate cells, were seen in TCDD-treated rats. Although the r
elevance of decreased ARAT activity under physiological conditions is
not clear, the changed LRAT activities most likely contributes signifi
cantly to the TCDD-induced effects on tissue retinyl ester levels. It
is intriguing that TCDD affects LRAT activity in hepatic stellate cell
s and kidney in opposite directions. The results suggest that effects
of TCDD on retinyl ester tissue levels could be due to a specific inte
raction with retinoid metabolism.