Flaxseed and its Lignan and Oil Components Reduce Mammary Tumor Growth at a Late Stage of Carcinogenesis

January 1, 1996 Human Health and Nutrition Data 0 Comments

Flaxseed and its Lignan and Oil Components Reduce Mammary Tumor Growth at a Late Stage of Carcinogenesis

Year: 1996
Authors: L U Thompson, S E Rickard, L J Orcheson, M M Seidl,
Publication Name: Carcinogenesis
Publication Details: Volume 17; Number 6; 1373.


Flaxseed has been shown to be protective at the early promotion stage of carcinogenesis. However, flaxseed is rich in both the mammalian lignan precursor secoisolariciresinol-diglycoside (SD) and ALA. The objective of the present study was to determine whether supplementation with flaxseed, its lignan or oil fractions, beginning 13 weeks after carcinogen administration, would reduce the size of established mammary tumors (present at the start of treatment) and appearance of new tumors in rats. Groups of 19-21 rats were given a singe dose of the carcinogen, 7,12-dimethylbenz[a[anthracene (DMBA) to stimulate tumor growth. After 13 weeks, rats were divided into five groups and were fed a basal diet (BD, 20% corn oil) or were supplemented with a gavage of 2200 nmol/day SD (SD- equal to the level in 5% flaxseed), 1.82% flaxseed oil (OIL – equal to the level in 5% flaxseed) or 2.5% or 5% flaxseed (2.5% flaxseed and 5% flaxseed, respectively). After 7 weeks of dietary treatment, established tumor volume was over 50% smaller in all treatment groups while there were no changes in the BD group. New tumor number and volume were significantly lower in the SD and 2.5% flaxseed groups. The combined established and new tumor volumes were significantly smaller for the SD, 2.5% flaxseed and 5% flaxseed groups compared to the OIL and BD groups. A significant negative correlation was reported between established tumor volume and urinary mammalian lignan excretion in the SD, 2.5% flaxseed and 5% flaxseed groups, indicating that mammalian lignans are effective in reducing established tumor growth. These results suggested to the authors that the reduction in tumor size noted was due in part to the lignans derived from the SD in the flaxseed. Because lignans have weak estrogenic/anti-estrogenic properties, the authors speculated that this reduction in tumor size may be due to an anti-estrogenic mechanism. There was no relationship between new or total tumor development and urinary lignan levels. Despite the lower urinary mammalian lignan excretion, SD was most effective in inhibiting new tumor development. The effect of flaxseed oil appeared to be related to its high ALA content. An increase in tumor cell peroxidation of ALA and longer chain n-3 PUFAs may have led to a decrease in cell viability. Lipid peroxidation products have also been shown to be toxic to tumor cells thereby suppressing their growth. The authors concluded that both the SD in flaxseed and ALA in flaxseed oil cause a reduction in carcinogenesis. However, the two components appear to affect different stages of cancer with SD being beneficial throughout the promotional phase of carcinogenesis and ALA being more effective at the stage when tumors have already been established. Further, the authors indicated that since SD feeding resulted in significantly lower urinary mammalian lignan levels in comparison to flaxseed, SD may not need to be fully metabolized to mammalian lignans to exert an anticarcinogenic effect.

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