RETINYL ESTER HYDROLASE AND VITAMIN A STATUS IN RATS TREATED WITH 3,3',4,4'-TETRACHLOROBIPHENYL

Previous studies have shown that rats exposed to 3,3′,4,4′-tetrachlorobiphenyl (TCB) exhibit decreased liver vitamin A stores. The activity of retinyl ester hydrolase (REH), the enzyme responsible for the hydrolysis of the storage form of vitamin A (retinyl esters) into free retinol, may therefore be altered by TCB. This study was carried out to investigate the effect of TCB on vitamin A distribution and on REH activity in the rat. REH activity was measured in liver homogenates and microsomes (650 μg protein), in Tris-maleate buffer 0.1 M at pH 7.2 in the presence of 150 mM CHAPS and 1.5 mM retinyl palmitate dispersed in Triton X-100 0.2%. Using these conditions, the kinetic parameters of the enzyme were determined and the inter-animal variation coefficient (10%) allowed statistical comparisons between experimental groups. Male Wistar rats of sufficient or deficient vitamin A status were treated IP with 340 fimol of TCB/kg. Vitamin A levels were significantly depressed in liver. REH activity was decreased about 20%, and serum retinol was decreased about 50%, independent of the initial vitamin A status of the animals. Vitamin A levels in lungs and testes were also decreased, suggesting that TCB could interfere with vitamin A delivery to target organs. The negative effect of TCB on REH activity in vivo was also observed when TCB was added in vitro to the incubation medium at concentrations near to those expected after in vivo treatment. TCB is a non-competitive inhibitor of retinyl palmitate hydrolase. © 1990.