INHIBITION OF 7,12-DIMETHYLBENZ(A)ANTHRACENE-INDUCED RAT MAMMARY CARCINOGENESIS BY CONCOMITANT OR POSTCARCINOGEN ANTIOXIDANT EXPOSURE

  • 1 January 1984
    • journal article
    • research article
    • Vol. 44  (7) , 2858-2863
Abstract
When administered prior to or at the time of carcinogen exposure, the phenolic antioxidants butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) are effective inhibitors of carcinogenesis in several target organs. However, chronic postcarcinogen administration of BHT apparently enhances tumorigenesis in certain animal models for liver and lung cancer. The present study was performed to determine the effects of BHA and BHT on mammary carcinogenesis when antioxidant exposure is limited to defined periods encompassing or following carcinogen availability. At 50 days of age (time 0), virgin female Sprague-Dawley rats (25/group) were given a single intragastric dose of 8 mg of 7,12-dimethylbenz(a)anthracene [DMBA]. Basal diet (Wayne Lab Meal) was supplemented with 5000 or 2500 mg of BHA or BHT/kg by the following protocol: 2 wk before until 1 wk after carcinogen administration; 1 wk after carcinogen administration until the end of the study; or none. When administered by the 2 wk before to 1 wk after schedule, both BHA and BHT were effective inhibitors of mammary carcinogenesis. However, the compounds were also active in chemoprevention when administered by the 1 wk after to end protocol. These data indicate that the anticarcinogenic activity of antioxidants is not limited to influences on carcinogen metabolism, since both BHA and BHT inhibited mammary tumor induction when their administration was begun following clearance of the carcinogen from the mammary gland. The anticarcinogenic activity of postcarcinogen administration of BHA and BHT in the mammary gland is in contrast to the apparent tumor-enhancing activity of BHT in the liver and lung.

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