BACKGROUND AND AIM: Ethanol has been shown to inhibit retinol oxidation at the level of alcohol dehydrogenase in liver and colon but not previously in the small intestine. In the present study we investigated how chronic alcohol feeding and acute ethanol exposure affects retinol dehydrogenase activity in the colon and small intestine of the rat. METHODS: Rats were fed ethanol in a liquid diet for six weeks. Control rats received a similar diet but with ethanol isocalorically replaced by carbohydrates. Retinol dehydrogenase was analyzed from cell cytosol samples from the small and the large intestine with respect to maximum activity (V(max)), Michaelis-Menten constant (K(m)), and inhibition by ethanol (2-43 mM) in vitro. RESULTS: Both the V(max) and the catalytic efficiency (V(max)/K(m)) were found to be significantly higher in the colon than in the small intestine (2.9-3.6 and 54-70 times higher, respectively). While chronic alcohol feeding did not affect these parameters, acute ethanol exposure reduced V(max) and V(max)/K(m) dose-dependently (p < 0.001) in both intestinal segments. CONCLUSION: The present data demonstrate that ethanol markedly inhibits in vitro cytosolic retinol oxidation in the small intestinal mucosa, which is considerably lower than that found in the colon. Considering the vital importance of retinol on intestinal integrity, our finding suggests that this might contribute to the ethanol-induced increase in intestinal permeability.
BACKGROUND AND AIM: Ethanol has been shown to inhibit retinol oxidation at the level of alcohol dehydrogenase in liver and colon but not previously in the small intestine. In the present study we investigated how chronic alcohol feeding and acute ethanol exposure affects retinol dehydrogenase activity in the colon and small intestine of the rat. METHODS:Rats were fed ethanol in a liquid diet for six weeks. Control rats received a similar diet but with ethanol isocalorically replaced by carbohydrates. Retinol dehydrogenase was analyzed from cell cytosol samples from the small and the large intestine with respect to maximum activity (V(max)), Michaelis-Menten constant (K(m)), and inhibition by ethanol (2-43 mM) in vitro. RESULTS: Both the V(max) and the catalytic efficiency (V(max)/K(m)) were found to be significantly higher in the colon than in the small intestine (2.9-3.6 and 54-70 times higher, respectively). While chronic alcohol feeding did not affect these parameters, acute ethanol exposure reduced V(max) and V(max)/K(m) dose-dependently (p < 0.001) in both intestinal segments. CONCLUSION: The present data demonstrate that ethanol markedly inhibits in vitro cytosolic retinol oxidation in the small intestinal mucosa, which is considerably lower than that found in the colon. Considering the vital importance of retinol on intestinal integrity, our finding suggests that this might contribute to the ethanol-induced increase in intestinal permeability.