EFFECTS OF ACUTE-INFLAMMATION ON PLASMA RETINOL, RETINOL-BINDING PROTEIN, AND ITS MESSENGER-RNA IN THE LIVER AND KIDNEYS OF VITAMIN-A-SUFFICIENT RATS

The acute inflammatory response to tissue injury and infection is asso ciated with low concentrations of plasma retinol and its specific tran sport proteins, retinol-binding protein (RBP) and transthyretin (TTR). To examine the kinetics and mechanism of hyporetinemia, we have induc ed acute inflammation with lipopolysaccharide (LPS, from Pseudomonas a eruginosa) in rats with adequate stores of vitamin A. Twenty-four h af ter treatment with LPS (50 mu g i.p. per 100 g body weight) or saline and food withdrawal, plasma retinol equalled 0.72 +/- 0.06 mu mol/L (m ean +/- SEM) in five LPS-treated rats versus 1.35 +/- 0.1 mu mol/L in five saline-treated rats (P<0.01). Plasma, liver, and kidney RBP and T TR concentrations were also significantly reduced, but liver and kidne y retinol concentrations did not differ between treatment groups. The relative abundance of RBP mRNA in liver (LPS treatment compared to sal ine treatment) was reduced as early as 12 h (0.44 +/- 0.15, n = 4 pair s, P<0.02), and continued to be reduced at 24 h (0.57 +/- 0.12, n = 5 pairs, P<0.02). In the kidney this ratio did not change significantly due to LPS treatment. The relative abundance of cellular retinol-bindi ng protein (CRBP) mRNA in liver and kidney also was not affected by LP S treatment. We infer from these data that inflammation-induced hypore tinemia results from a reduction in the hepatic synthesis of RBP and s ecretion of the retinol-RBP complex. Moreover, the results imply that plasma retinol concentration is a poor indicator of vitamin A status d uring inflammation.-Rosales, F. J., S. J. Ritter, R. Zolfaghari, J. E. Smith, and A. C. Ross. Effects of acute inflammation on plasma retino l, retinol-binding protein, and its mRNA in the liver and kidneys of v itamin A-sufficient rats.