Experiments on Wistar rats showed that feeding a ration containing 0.1% concentrate of food indoles (indole-3-carbinole and ascorbigen) for 3 weeks increased activity of phases I and II xenobiotic metabolism enzymes in the liver and intestinal mucosa and weakened the toxic effects of trichothecene T-2 mycotoxin. Activity of the key enzymes of T-2 detoxification, microsomal carboxylesterase and UDP-glucuronosyl transferase, was 1.5-2-fold higher in rats receiving T-2 toxin against the background of indole-enriched diet compared to toxin-treated rats kept on standard ration.

Oral treatment with lycopene (per os) in doses of 10 or 50 mg/kg for 2 weeks led to accumulation of lycopene in the liver, liver microsomes, and blood plasma, increased total plasma antioxidant activity, inhibited LPO in the liver, and decreased solubilization of lysosomal enzymes. Lycopene had no effect on ex vivo resistance of liver microsomes to LPO and activities of antioxidant enzymes in the liver.

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Male Wistar rats received a semisynthetic diet with resveratrol (100 mg/kg), indole-3-carbinol (20 mg/kg), or a mixture of these compounds in the same doses for 1 week. Activities of ethoxyresorufin dealkylase (EROD), methoxyresorufin dealkylase (MROD), pentoxyresorufin dealkylase (PROD), and 6β-testosterone hydroxylase (6β-TH) and the content of mRNA for CYP1A1, CYP1A2, and CYP3A1 were elevated in the liver of rats receiving indole-3-carbinol. These changes were accompanied by an increase in activity of phase II xenobiotic metabolism enzymes (quinone reductase, hemoxygenase-1, glutathione transferase, and UDP glucuronosyl transferase). Resveratrol did not modify activity of these enzymes. After combined treatment with the test compounds, resveratrol suppressed the indole-3-carbinol-induced increase in activities of EROD, MROD, PROD, and 6β-TH, and expression of the corresponding genes. Combined treatment was characterized by potentiation of the antioxidant effects of these compounds.