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Shertzer HG, Niemi MP, Reitman FA, et al. Protection against carbon tetrachloride hepatotoxicity by pretreatment with indole-3-carbinol. Exp Mol Pathol. 1987;46(2):180-9doi: 10.1016/0014-4800(87)90064-5.
Shertzer, H. G., Niemi, M. P., Reitman, F. A., Berger, M. L., Myers, B. L., & Tabor, M. W. (1987). Protection against carbon tetrachloride hepatotoxicity by pretreatment with indole-3-carbinol. Experimental and molecular pathology, 46(2), 180-9. https://doi.org/10.1016/0014-4800(87)90064-5
Shertzer, H G, et al. "Protection against carbon tetrachloride hepatotoxicity by pretreatment with indole-3-carbinol." Experimental and molecular pathology vol. 46,2 (1987): 180-9. doi: https://doi.org/10.1016/0014-4800(87)90064-5
Shertzer HG, Niemi MP, Reitman FA, Berger ML, Myers BL, Tabor MW. Protection against carbon tetrachloride hepatotoxicity by pretreatment with indole-3-carbinol. Exp Mol Pathol. 1987 Apr;46(2):180-9. doi: 10.1016/0014-4800(87)90064-5. PMID: 3556531.
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Elsevier Science

Exp Mol Pathol. 1987 Apr;46(2):180-9. doi: 10.1016/0014-4800(87)90064-5.

Protection against carbon tetrachloride hepatotoxicity by pretreatment with indole-3-carbinol.

Experimental and molecular pathology

H G Shertzer, M P Niemi, F A Reitman, M L Berger, B L Myers, M W Tabor

PMID: 3556531 DOI: 10.1016/0014-4800(87)90064-5

Abstract

The effects of administering indole-3-carbinol (I-3-C) on carbon tetrachloride (CCl4)-induced hepatotoxicity were examined. Mice received by gavage 0-150 mg I-3-C/kg body wt in methanol-extracted corn oil, followed 1 h later by 15 microliters CCl4/kg body wt in corn oil. Animals were sacrificed 24 h after receiving CCl4. Pretreatment with I-3-C reduced the degree of centrolobular necrosis, as observed histologically. Additionally, CCl4-mediated elevated serum enzymes were reduced by I-3-C. Although I-3-C induced elevated levels of cytochrome P-450 and associated mixed-function oxidase activity, the CCl4 depression of these parameters was not clearly reversed by I-3-C. However, CCl4 produced decreases in hepatic levels of glutathione (GSH), total reducing equivalents, and protein sulfhydryls, all of which were restored to control levels by I-3-C. Using mouse liver microsomes in an NADPH-fortified reaction mixture, I-3-C inhibited, in a concentration-dependent manner, CCl4-initiated lipid peroxidation, with 50% inhibition at 35-40 microM I-3-C. When mice were treated by gavage with 50 mg [14C]I-3-C/kg body wt, concentrations of radiolabel in the liver were greater than 100 microM after 1 hr. This was five times the level of radioactivity measured in blood and three times the concentration of I-3-C necessary for 50% inhibition of CCl4-mediated lipid peroxidation in vitro. The data are consistent with the hypothesis that I-3-C intervenes in CCl4-mediated hepatic necrosis by combining with reactive free radical metabolites of CCl4, thereby protecting critical cellular target sites.

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