The effect of iron on experimental colorectal carcinogenesis

Anticancer Res. 1989 Nov-Dec;9(6):1477-82.

Abstract

The effect of parenteral and oral iron was examined in the rat 1,2 dimethylhydrazine (DMH) colorectal carcinogenesis model in a series of experiments. Parenteral supplementation of iron was found to augment tumor yield (p = 0.012) and oral iron was found to augment tumor incidence (p = 0.03, when control groups were combined). In addition, phytic acid, a significant component of dietary fiber was found to reverse the augmenting effect of oral iron on tumor yield and incidence (p = 0.09 for both). Furthermore, in a short term DMH nuclear toxicity assay, analysis of the karyorrhectic index (KI), there was no difference in the KI between oral iron and phytate dietary groups (p = 0.53 for the left colon and p = 0.2 for the right colon), implying that iron's effect on colorectal tumor induction takes place during the promotional phase of carcinogenesis and not during initiation. These experiments support the epidemiologic observation that dietary iron may augment colorectal cancer risk and that the mechanism by which dietary fiber diminishes colorectal cancer risk may be the chelation of dietary iron by the phytic acid component of dietary fiber.

MeSH terms

  • 1,2-Dimethylhydrazine
  • Animals
  • Carcinogens*
  • Colon / drug effects
  • Colon / pathology*
  • Colonic Neoplasms / chemically induced
  • Colonic Neoplasms / pathology*
  • Colonic Neoplasms / prevention & control
  • Dietary Fiber / therapeutic use*
  • Dimethylhydrazines
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / pathology
  • Iron-Dextran Complex / toxicity*
  • Karyotyping
  • Rats
  • Rats, Inbred Strains
  • Rectal Neoplasms / chemically induced
  • Rectal Neoplasms / pathology*
  • Rectal Neoplasms / prevention & control

Substances

  • Carcinogens
  • Dietary Fiber
  • Dimethylhydrazines
  • Iron-Dextran Complex
  • 1,2-Dimethylhydrazine