Potency of dietary indole-3-carbinol as a promoter of aflatoxin B1-initiated hepatocarcinogenesis: results from a 9000 animal tumor study.
Level 5 - mechanism / opinion, no new human data
Animal model study (rainbow trout)
PubMed 10190561 · doi:10.1093/carcin/20.3.453
What was done
Approximately 9,000 rainbow trout embryos were initiated with aflatoxin B1 (AFB1) at concentrations of 0, 25, 50, 100, 175, or 250 p.p.b. for 30 minutes. Starting at 3 months of age, fish were fed experimental diets containing 0, 250, 500, 750, 1000, or 1250 p.p.m. indole-3-carbinol (I3C). Fish were sampled for liver tumors at 11 to 13 months. Biomarkers of estrogenic activity (vitellogenin induction) and Ah receptor activity (CYP1A induction) were also evaluated.
What was found
Dietary I3C given post-initiation caused statistically significant promotion of liver tumor incidence at all tested dietary levels of 500 p.p.m. and higher, but not at 250 p.p.m. Promotion potency increased markedly above 750 p.p.m. Vitellogenin was induced at 250 p.p.m. and above, whereas CYP1A was induced only at 1000 p.p.m. and above, with the strongest promotion observed at 1000 and 1250 p.p.m. where both pathways were active. The abstract reports no exact numeric tumor incidence rates or percentages.
Why it matters
These findings show that indole-3-carbinol, commonly considered a dietary chemopreventive agent from cruciferous vegetables, can act as a potent promoter of hepatocarcinogenesis when given after carcinogen exposure.
Limits
The study was performed entirely in rainbow trout, limiting direct translation to mammalian or human physiology. Specific quantitative tumor incidences, confidence intervals, and survival metrics are not reported in the abstract.
Cited by
- supports Animal studies of indole-3-carbinol (I3C) have shown that whether it prevents or promotes cancer depends on whether it is administered before or after exposure to a carcinogen.