Indole-3-carbinol inhibits lipid peroxidation in cell-free systems.

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 hepatotoxicity 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.