Indole-3-carbinol Inhibits Lipid Peroxidation in Cell-Free Systems

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Abstract
Free radicals mediate toxicological and carcinogenic responses of tissues to many chemicals. Cellular defenses against radical mediated damage utilize endogenous substances such as tocopherol, ascorbate and GSH.Here we report a new antioxidant, indole-3-carbinol (I-3-C), a natural constituent of human diet.In chlorobenzene containing soy phospholipids, lipid oxidation was initiated with azobisisobutyronitrile; I-3-C inhibited formation of thiobarbituric acid-reactive material in a dose-dependent manner. Similar results were obtained in an aqueous system containing phospholipid vesicles initiated by Fe/ascorbate. For both systems I-3-C was less effective than tocopherol or BHT as antioxidant. To assess these antioxidant effects in vivo, mice were treated with I-3-C by gavage. A hepatic post-mitochondrial supernatant fraction isolated 2 hours after treatment showed dose-dependent decreases in NADPH-mediated lipid oxidation which correlated with decreases in 14C-nitrosodimethylamine covalent binding to protein. Although hepato-toxicity may not involve lipid oxidation per se, it does indicate that free radical damage had occurred. Inhibition of damage by I-3-C suggests that this dietary component has the potential to ameliorate radical mediated chemical toxicity.

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