Title | Low-dose dietary chlorophyll inhibits multi-organ carcinogenesis in the rainbow trout. |
Publication Type | Journal Article |
Year of Publication | 2008 |
Authors | Simonich MT, McQuistan T, Jubert C, Pereira C, Hendricks JD, Schimerlik M, Zhu B, Dashwood RH, Williams DE, Bailey GS |
Journal | Food Chem Toxicol |
Volume | 46 |
Issue | 3 |
Pagination | 1014-24 |
Date Published | 2008 Mar |
ISSN | 0278-6915 |
Keywords | Animals, Benzopyrenes, Chlorophyll, Diet, Electron Spin Resonance Spectroscopy, Neoplasms, Multiple Primary, Oncorhynchus mykiss, Tissue Distribution |
Abstract | We recently reported that chlorophyll (Chl) strongly inhibits aflatoxin B(1) preneoplasia biomarkers in rats when administered by co-gavage (Simonich et al., 2007. Natural chlorophyll inhibits aflatoxin B1-induced multi-organ carcinogenesis in the rat. Carcinogenesis 28, 1294-1302.). The present study extends this by examining the effects of dietary Chl on tumor development, using rainbow trout to explore ubiquity of mechanism. Duplicate groups of 140 trout were fed diet containing 224 ppm dibenzo[a,l]pyrene (DBP) alone, or with 1000-6000 ppm Chl, for 4 weeks. DBP induced high tumor incidences in liver (51%) and stomach (56%), whereas Chl co-fed at 2000, 4000 or 6000 ppm reduced incidences in stomach (to 29%, 23% and 19%, resp., P<0.005) and liver (to 21%, 28% and 26%, resp., P<0.0005). Chlorophyllin (CHL) at 2000 ppm gave similar protection. Chl complexed with DBP in vitro (2Chl:DBP, K(d1)=4.44+/-0.46 microM, K(d2)=3.30+/-0.18 microM), as did CHL (K(d1)=1.38+/-0.32 microM, K(d2)=1.17+/-0.05 microM), possibly explaining their ability to inhibit DBP uptake into the liver by 61-63% (P<0.001). This is the first demonstration that dietary Chl can reduce tumorigenesis in any whole animal model, and that it may do so by a simple, species-independent mechanism. |
DOI | 10.1016/j.fct.2007.10.034 |
Alternate Journal | Food Chem. Toxicol. |
PubMed ID | 18069110 |
PubMed Central ID | PMC2404114 |
Grant List | CA 90890 / CA / NCI NIH HHS / United States P01 CA090890 / CA / NCI NIH HHS / United States P30 ES003850 / ES / NIEHS NIH HHS / United States P01 CA090890-04 / CA / NCI NIH HHS / United States ES 03850 / ES / NIEHS NIH HHS / United States ES 00210 / ES / NIEHS NIH HHS / United States P30 ES000210-40 / ES / NIEHS NIH HHS / United States P30 ES003850-15 / ES / NIEHS NIH HHS / United States P30 ES000210 / ES / NIEHS NIH HHS / United States |