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Excess Vitamin A Decreases the Specific Activity of Galactosyltransferase in Golgi Apparatus of Rat Liver^1,2,

Department of Foods and Nutrition, Purdue University, West Lafayette, IN 47907

This study investigated the effects of vitamin A excess on hepatic galactosyltransferase (EC 2.4.1.13) activity in livers of rats achieved either by feeding of high levels of retinyl palmitate for 16 wk or gavaging with retinol in olive oil for 3 d. Both hypervitaminotic conditions were characterized by hepatic lipid accumulation. Golgi apparatus fractions were isolated and purity of the fractions was monitored by marker-enzyme analyses and electron microscopy. The quality of the fractions isolated from livers of rats receiving vitamin A excess was not different from that of fractions from control rats. An increase in fat-storing cells in liver, observed in vitamin A excess, coincided with the presence of a floating lipid layer present during isolation of the Golgi apparatus. Galactosyltransferase specific activity (with ovomucoid as acceptor) of Golgi apparatus of rats fed excess vitamin A was 27% of control with chronic feeding and 59% of control with administration by gavage. Activity of another luminally oriented protein, uridine 5'-diphosphate phosphatase, was increased under both in vivo regimens. Vitamin A content of Golgi apparatus, as determined by high performance liquid chromatography, correlated negatively with galactosyltransferase activity after both chronic and acute administration of excess vitamin A.

KEY WORDS: • vitamin A • Golgi apparatus • liver • rats

¹ Supported in part by Phi Beta Psi Sorority and Purdue Research Foundation, 8546-561264 Paper No. 11444 of the Purdue University Agricultural Experiment Station, West Lafayette, IN 47907.

² Presented in part at the annual meeting of the American Society for Cell Biology, Washington, DC, December, 1986 [Martin, B. R. & Morré, D. M. (1986) Effect of excess vitamin A on hepatic Golgi apparatus in rats. J. Cell Biol. 103: 64 (abs.)].

³ To whom correspondence and reprint requests should be sent.

Manuscript received 2 February 1988. Revision accepted 13 April 1988.