Studies on the preventive effect of red palm oil on 17ẞ-estradiol epoxidation and the potential against breast cancer carcinogenesis at the initiation

Yu, Fu-Li. and Abdul Gapor, . and Bender, Wanda (2005) Studies on the preventive effect of red palm oil on 17ẞ-estradiol epoxidation and the potential against breast cancer carcinogenesis at the initiation. [Proceedings Paper]

Epidemiological studies have indicated that estrogens are involved in breast cancer. However, the mechanism is still not fully understood. We found that 17ẞ-estradiol (E₂) could be activated by the versatile epoxide-forming oxidant dimethyldioxirane (DMDO) to inhibit nuclear RNA synthesis and to bind DNA forming DNA adducts both in vitro and in vivo. Since DNA adducts can cause mutation, and mutation is the molecular basis for the initiation of carcinogenesis, we proposed E₂ epoxidation is the underlying mechanism for the initiation of breast cancer. Based on this new insight, a method to screen chemopreventive agents against breast cancer, at the initiation, was developed. This screening test determines whether a chemical is able to prevent the formation of E₂ epoxide as measured by both the loss of the ability of E₂ to inhibit nuclear RNA synthesis and the ability of [3H]labeled E₂ to bind to DNA. Red Palm Oil (RPO), rich in carotenoids, tocopherols and tocotrienols, may have protective effects against vitamin A deficiency, cardiovascular diseases, and cancer including breast cancer. This report is to examine the transcriptional and DNA binding properties of RPO, and its preventive effect on E₂ epoxidation. We found that RPO, unlike E₂ could not be activated by DMDO to inhibit nuclear RNA synthesis. Therefore, it is not genotoxic. However, when incubated together with E₂ for epoxidation by DMDO, RPO was able to strongly prevent the formation of E₂ epoxide as reflected by the loss of the ability of E₂ to inhibit nuclear RNA synthesis. Additionally, we found that RPO was able to prevent the binding of [H]labeled E₂ to DNA in a dose- dependent manner. This preventive effect of RPO on the binding of E₂ to DNA was further confirmed when liver microsomes were used for the activation. We believe that this is the first report on the transcriptional and DNA binding properties of RPO, and its inhibitory effect on the formation of E₂ epoxide. As a dietary supplement, RPO may have the potential to prevent E₂ induced breast cancer carcinogenesis at the initiation.

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Abstract

Epidemiological studies have indicated that estrogens are involved in breast cancer. However, the mechanism is still not fully understood. We found that 17ẞ-estradiol (E₂) could be activated by the versatile epoxide-forming oxidant dimethyldioxirane (DMDO) to inhibit nuclear RNA synthesis and to bind DNA forming DNA adducts both in vitro and in vivo. Since DNA adducts can cause mutation, and mutation is the molecular basis for the initiation of carcinogenesis, we proposed E₂ epoxidation is the underlying mechanism for the initiation of breast cancer. Based on this new insight, a method to screen chemopreventive agents against breast cancer, at the initiation, was developed. This screening test determines whether a chemical is able to prevent the formation of E₂ epoxide as measured by both the loss of the ability of E₂ to inhibit nuclear RNA synthesis and the ability of [3H]labeled E₂ to bind to DNA. Red Palm Oil (RPO), rich in carotenoids, tocopherols and tocotrienols, may have protective effects against vitamin A deficiency, cardiovascular diseases, and cancer including breast cancer. This report is to examine the transcriptional and DNA binding properties of RPO, and its preventive effect on E₂ epoxidation. We found that RPO, unlike E₂ could not be activated by DMDO to inhibit nuclear RNA synthesis. Therefore, it is not genotoxic. However, when incubated together with E₂ for epoxidation by DMDO, RPO was able to strongly prevent the formation of E₂ epoxide as reflected by the loss of the ability of E₂ to inhibit nuclear RNA synthesis. Additionally, we found that RPO was able to prevent the binding of [H]labeled E₂ to DNA in a dose- dependent manner. This preventive effect of RPO on the binding of E₂ to DNA was further confirmed when liver microsomes were used for the activation. We believe that this is the first report on the transcriptional and DNA binding properties of RPO, and its inhibitory effect on the formation of E₂ epoxide. As a dietary supplement, RPO may have the potential to prevent E₂ induced breast cancer carcinogenesis at the initiation.

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Item Type:	Proceedings Paper
Additional Information:	Available at Perpustakaan Sultan Abdul Samad, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia. TP684 P3I61 2005 Call Number
AGROVOC Term:	palm oils
AGROVOC Term:	Cancer (genus)
AGROVOC Term:	disease prevention
AGROVOC Term:	antioxidants
AGROVOC Term:	estradiol
AGROVOC Term:	carcinogenesis
AGROVOC Term:	chemoprophylaxis
Geographical Term:	Malaysia
Depositing User:	Nor Hasnita Abdul Samat
Date Deposited:	01 Nov 2025 11:47
Last Modified:	10 Nov 2025 01:09
URI:	http://webagris.upm.edu.my/id/eprint/1229

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