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2004 NOV 4 - (NewsRx.com & NewsRx.net) -- University of Illinois researchers say oleic acid could be a potential initiating carcinogen after epoxidation of 17beta-estradiol, a mechanism they previously suggested results in breast cancer carcinogenesis.
"The effect of dietary fat on breast cancer is a long-standing and an unresolved issue. We found that 17beta-estradiol (E-2) could be activated by the epoxide-forming oxidant dimethyldioxirane (DMDO) to bind DNA-forming DNA adducts both in vitro and in vivo, and to inhibit nuclear RNA synthesis. We proposed that E-2 epoxidation is the underlying mechanism for the initiation of breast cancer carcinogenesis (Carcinogenesis, 1996;17:1957-61)," wrote F.L. Yu and colleagues.
Their current study looked at "the transcriptional and DNA-binding properties of vegetable oils and fatty acids, and on the potentials of these compounds to prevent the formation of E-2 epoxide."
Yu and associates found that "vegetable oils, having no effect on nuclear RNA synthesis either before or after DMDO treatment, were all able to prevent the formation of E-2 epoxide independent of their mono- or polyunsaturated fatty acid content."
"Similarly," they reported, "unsaturated fatty acids, regardless of chain length and number of double bonds, were all able to prevent the formation of E-2 epoxide as reflected by the loss of the ability of [H-3]E-2 to bind DNA.
"In contrast to vegetable oils, the results indicated that the unsaturated fatty acids palmitoleic, oleic, linoleic, linolenic, and arachidonic acid could be activated by DMDO to inhibit ...