Dietary chlorophyllin is a potent inhibitor of aflatoxin B1 hepatocarcinogenesis in rainbow trout.

نویسندگان

  • V Breinholt
  • J Hendricks
  • C Pereira
  • D Arbogast
  • G Bailey
چکیده

Epidemiological and experimental evidence indicates a strong relationship between diet and cancer. The purpose of this study was to examine the potential of chlorophyllin (CHL), a food-grade derivative of the ubiquitous green plant pigment chlorophyll, to inhibit experimental carcinogenesis. We report that CHL is a potent, dose-responsive inhibitor of aflatoxin B1 DNA adduction and hepatocarcinogenesis in the rainbow trout model when fed with carcinogen. CHL neither promoted nor suppressed carcinogenesis with chronic postinitiation feeding. By molecular dosimetry analysis, reduced aflatoxin B1-DNA adduction accounted quantitatively for reduced tumor response up to 2000 ppm dietary CHL, but an additional protective mechanism was operative at 4000 ppm CHL. The finding of potent inhibition (up to 77%) at CHL levels well within the chlorophyll content of some green leafy vegetables may have important implications in intervention and dietary management of human cancer risks.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Using salmonid microarrays to understand the dietary modulation of carcinogenesis in rainbow trout.

The highlighted article in this issue by Tilton et al. (2005a) is an innovative approach to evaluate the modulation of estrogen receptor (ER) and aryl hydrocarbon (Ah)-receptor pathways as mechanisms underlying indole-3-carbinol (I3C) tumor promotion in rainbow trout (Onchorhynchus mykiss). I3C and its major in vivo component 3,3'-diindolylmethane (DIM) are potent tumor promoters that appear to...

متن کامل

Purified form of cytochrome P-450 from rainbow trout with high activity toward conversion of aflatoxin B1 to aflatoxin B1-2,3-epoxide.

Aflatoxin B1, the most potent hepatic chemical carcinogen known, is activated to the putative product aflatoxin B1-2,3-epoxide via a cytochrome P-450-dependent reaction. Mt. Shasta rainbow trout is the most sensitive species known to the hepatocarcinogenic effects of aflatoxin B1. We have previously isolated and purified a minor form of cytochrome P-450 from this strain of rainbow trout, with a...

متن کامل

Simultaneous effect of stocking density, dietary aflatoxin B1 and medicinal plant multi-blend on digestive physiology of rainbow trout (Oncorhynchus mykiss)

The effect of stocking density and dietary aflatoxin B1 along with including rosemary and thyme powders on digestive enzymes activity of rainbow trout was evaluated. 600 fish with an average weight of 90±3 were randomly allotted into six experimental groups consisted of (1) stocking at 15 kg.m-3- feeding diet devoid of aflatoxin, (2) stocking at 45 kg.m-3-feeding diet devoid of aflatoxin, (3) s...

متن کامل

Purified Form of Cytochrome P-450 from Rainbow Trout with High Activity toward Conversion of Aflatoxin B1 to Aflatoxin Br 2,3-epoxide1

Aflatoxin Bi, the most potent hepatic chemical carcinogen known, is activated to the putative product aflatoxin B,-2,3epoxide via a cytochrome P-450-dependent reaction. Mt. Shasta rainbow trout is the most sensitive species known to the hepatocarcinogenic effects of aflatoxin B,. We have previously iso lated and purified a minor form of cytochrome P-450 from this strain of rainbow trout, with a...

متن کامل

Enhancement of aflatoxin B1 and N-methy1-N'- nitro-N-nitrosoguanidine hepatocarcinogenesis in rainbow trout Salmo gairdneri by 17-B-estradiol and other organic chemicals*

Twenty-one-day-old rainbow trout Salmo gairdneri embryos were exposed to static solutions of aflatoxin B, (AFB,) (0.5 pprn for 30 min) or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) (50 ppm for 60 min) to initiate neoplasms of the liver (AFB1 and MNNG) and other organs (MNNG). Ten weeks after the onset of feeding (14 wk after carcinogen exposure) the fish were started on diets containing 500 pp...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Cancer research

دوره 55 1  شماره 

صفحات  -

تاریخ انتشار 1995