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.
CITATION STYLE
Shertzer, H. G., Niemi, M. P., & Tabor, M. W. (1986). Indole-3-carbinol inhibits lipid peroxidation in cell-free systems. Advances in Experimental Medicine and Biology, 197, 347–356. https://doi.org/10.1007/978-1-4684-5134-4_32
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