Aging : increased responsiveness of colorectal mucosa to carcinogen stimulation and protective role of folic acid

Recent investigations have demonstrated a protective role for folic acid in dysplasia and neoplasia, through an unknown mechanism. The current study was designed to evaluate whether the protective role of folic acid is due, in part, to its antiproliferative properties. In addition, because colorecta...

Full description

Saved in:
Bibliographic Details
Published in:Digestive diseases and sciences 1995-02, Vol.40 (2), p.396-401
Main Authors: NENSEY, Y. M, ARLOW, F. L, MAJUMDAR, A. P. N
Format: Article
Language:English
Subjects:
Aging - drug effects
Aging - metabolism
Analysis of Variance
Animals
Biological and medical sciences
Carcinogenesis, carcinogens and anticarcinogens
Colon - chemistry
Colon - drug effects
Colon - enzymology
Folic Acid - pharmacology
Foods and miscellaneous
Intestinal Mucosa - chemistry
Intestinal Mucosa - drug effects
Intestinal Mucosa - enzymology
Male
Medical sciences
Methylazoxymethanol Acetate - pharmacology
Organ Culture Techniques
Ornithine Decarboxylase - analysis
Ornithine Decarboxylase - drug effects
Pilot Projects
Protein-Tyrosine Kinases - analysis
Protein-Tyrosine Kinases - drug effects
Rats
Rats, Inbred F344
Rectum - chemistry
Rectum - drug effects
Rectum - enzymology
Specific Pathogen-Free Organisms
Tumors
Citations: Items that this one cites
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Recent investigations have demonstrated a protective role for folic acid in dysplasia and neoplasia, through an unknown mechanism. The current study was designed to evaluate whether the protective role of folic acid is due, in part, to its antiproliferative properties. In addition, because colorectal neoplasia is more common with increasing age, we have compared results in both old (22 months) and young (3 months) rats. Colorectal mucosal explants of rats treated with the known carcinogen methylazoxymethanol, were supplemented with folic acid. Ornithine decarboxylase was then measured as an index of cellular proliferative activity. We observed that supplemental folic acid suppressed carcinogen-induced ornithine decarboxylase activity by 64% in the old and 74% in the young rats. Furthermore, a similar phenomenon was observed for tyrosine kinase, which was measured for comparison. The suppression of hyperproliferative activity by supplemental folic acid may contribute to the protective effect of folic acid in colorectal neoplasia.
ISSN:0163-2116
1573-2568
DOI:10.1007/bf02065427