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Differential Effects of Retinoids and Chronic Ethanol Consumption on Membranes in Rats¹

Alcohol Research and Treatment Center, Section of Liver Disease and Nutrition, Veterans Administration Medical Center, Bronx, NY 10468 and Mount Sinai School of Medicine (CUNY), New York, NY 10029

Liver plasma membranes (LPM) were prepared from vitamin A—deficient and — sufficient rats as well as from animals treated with retinoic acid, with or without ethanol. Although the fluorescence polarization value of LPM prepared from retinoic acid—fed animals was significantly lower than that of controls (0.201 ± 0.008 vs. 0.254 ± 0.005, P < 0.001), no effect was seen with a vitamin A—deficient diet (0.259 ± 0.005). No change in the fluorescence polarization was observed in erythrocyte ghost membranes with either vitamin A deficiency or chronic ethanol consumption. The sialic acid concentration of the membranes was significantly higher in LPM and erythrocyte ghosts obtained from vitamin A—deficient animals (37.6 ± 1.1 vs. 29.6 ± 0.7 nmol/mg protein for LPM, P < 0.01, and 77.7 ± 0.6 vs. 62.0 ± 1.7 for erythrocyte ghosts, P < 0.001); the LPM of retinoic acid—treated animals had the lowest values (26.9 ± 1.6 nmol/mg protein). This sialic acid concentration of LPM was positively correlated with the fluorescence polarization (r = 0.775, P < 0.001). Chronic ethanol feeding resulted in lower hepatic and LPM vitamin A and greater LPM fluidity with higher cholesterol esters in all diet groups (P < 0.001). Because increased sialic acid concentration has been incriminated in the pathogenesis of tumor development, it may provide a mechanism whereby lowered hepatic vitamin A promotes carcinogenesis and retinoic acid feeding opposes this process.

KEY WORDS: • vitamin A deficiency • ethanol • membranes • sialic acid • retinoic acid

¹ This study was supported by Department of Health and Human Services Grants No. DK 32810, No. AA 03508 and No. AA 05934 and by the Veterans Administration.

² To whom reprint requests should be addressed.

Manuscript received 6 January 1988. Revision accepted 6 May 1988.

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