Title of article :
Inhibition by dietary dibenzoylmethane of mammary gland proliferation, formation of DMBA–DNA adducts in mammary glands, and mammary tumorigenesis in Sencar mice
Author/Authors :
Lin، نويسنده , , Chuan-Chuan and Lu، نويسنده , , Yao-Ping and Lou، نويسنده , , You-Rong and Ho، نويسنده , , Chi-Tang and Newmark، نويسنده , , Harold H and MacDonald، نويسنده , , Christopher and Singletary، نويسنده , , Keith W and Huang، نويسنده , , Mou-Tuan، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2001
Pages :
8
From page :
125
To page :
132
Abstract :
Dibenzoylmethane (DBM) is a minor constituent of licorice and a β-diketone analogue of curcumin. Feeding 1% DBM in the diet to Sencar mice during both the initiation and the post-initiation periods strongly inhibited 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary tumor multiplicity and mammary tumor incidence by 97%. In further in vivo studies to elucidate the possible mechanisms of the inhibitory action of DBM, feeding the 1% DBM in the AIN-76A diet to immature Sencar mice for 4–5 weeks decreased the uterine wet weight by 43%, inhibited the proliferation rate of mammary gland epithelial cells by 53%, uterine epithelium by 23%, and uterine stroma by 77%, when mice were killed during the first estrus phase of estrous cycle. In addition, feeding 1% DBM in the diet to Sencar mice at 2 weeks before, during and 1 week after DMBA treatment (intubation of 1 mg DMBA per mouse once a week for 5 weeks) inhibited formation of total DMBA–DNA adducts in mammary glands by 72% using a post-32P-labeling assay. Thus, feeding 1% DBM diet to Sencar mice inhibited formation of DMBA–DNA adducts in mammary glands and lowered the proliferation rate of the mammary gland in vivo. These results may explain the strong inhibitory actions of dietary DBM on mammary carcinogenesis in mice.
Keywords :
Prevention , Dibenzoylmethane , Curcumin , ?-diketone , mammary tumorigenesis
Journal title :
Cancer Letters
Serial Year :
2001
Journal title :
Cancer Letters
Record number :
1802731
Link To Document :
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