1. Ethanol enhances retinoic acid metabolism into polar metabolites in rat liver via induction of cytochrome P4502E1 
Chun Liu, Robert M. Russell, Helmut K. Seitz, Xiang -Dong Wang 
Gastroenterology 
Volume 120, Issue 1, Pages (January 2001)
DOI: /gast
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2. Fig. 1
Effects of chlormethiazole (a specific CYP2E1 inhibitor) and liarozole (a nonspecific CYP enzyme inhibitor) on RA metabolism. HPLC analysis of retinoids in the rat liver microsomal fraction (LMF) after incubation with 1 μmol/L RA: (A) retinoid standards, (B) ethanol-exposed LMF without either inhibitor, (C) ethanol-exposed LMF with chlormethiazole, (D) ethanol-exposed LMF with liarozole, and (E) control (non–ethanol-exposed LMF without inhibitor). Peak identifications: (1) 4-oxo-RA, (2) 18-hydroxy-RA, (3) RA, (4) retinol, and (5) retinyl acetate (internal standard).
Gastroenterology  , DOI: ( /gast )
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3. Fig. 2
The spectra of compounds (A, peak 1 from Figure 1; C, peak 2 from the Figure 1) derived from the incubation of RA and the spectra of authentic (B) 4-oxo-RA and (D) 18-hydroxy-RA.
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

4. Fig. 3
Effects of increasing (A) microsomal protein concentration and (B) substrate concentration on both 18-hydroxy-RA and 4-oxo-RA syntheses derived from RA incubated with the microsomal fractions of livers from ethanol-fed rats (●) and non–ethanol-fed rats (○). The experimental conditions are described in Materials and Methods. Each point represents the average of 2 separate experiments.
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

5. Fig. 4
Effect of chronic ethanol intake on the expression of CYP2E1, CYP1A2, and CYP3A1 in rat liver microsomes. Representative Western blot analysis for CYP2E1, CYP1A2, and CYP3A1 from 3 pair-fed rats (C, control; E, ethanol) is shown. The sizes of the detected CYP2E1, CYP1A2, and CYP3A1 were 51, 55, and 48 kilodaltons, respectively. The method is as described in Materials and Methods.
Gastroenterology  , DOI: ( /gast )
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6. Fig. 5
Inhibitory effects of (A) chlormethiazole and (B) allylsulfide on RA metabolism in ethanol-fed rat microsomal fractions. The experimental conditions are described in Materials and Methods. Each point represents the average of 2 separate experiments.
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions

7. Fig. 6
Inhibitory effects of chlormethiazole on RA metabolism in ethanol-fed rat microsomal fractions. (A) Plot of enzymatic activity vs. RA concentration in the presence (●) and absence (○) of chlormethiazole (100 μmol/L). (B) Lineweaver–Burk plots of 18-hydroxy-RA formation from RA oxidation in ethanol-fed rat microsomal fractions with or without chlormethiazole. The data are plotted as the reciprocal of the reaction rate (pmol · min−1 · mg protein−1) and as the reciprocal of the RA concentration (μmol/L). The apparent Km and Vmax are 2.94 μmol/L and 5.9 pmol · min−1 · mg protein−1 for 18-hydroxy-RA formation from RA oxidation in ethanol-fed rat microsomal fractions without and 2.98 μmol/L and 2.4 pmol · min−1 · mg protein−1 with chlormethiazole.
Gastroenterology  , DOI: ( /gast )
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8. Fig. 7
Inhibitory effect of antibody against CYP2E1 on the formation of (A) 18-hydroxy-RA and (B) 4-oxo-RA from RA in ethanol-treated and non–ethanol-treated rats. The incubation procedure was as described in Materials and Methods. The antibody was preincubated for 10 minutes before the initiation of reaction. Data are means ± SE (n = 3–4; *P < 0.05).
Gastroenterology  , DOI: ( /gast )
Copyright © 2001 American Gastroenterological Association Terms and Conditions