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J. Biol. Chem., Vol. 279, Issue 11, 10670-10676, March 12, 2004

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Inhibition of AP-1 and Neoplastic Transformation by Fresh Apple Peel Extract^*

Min Ding, Yongju Lu, Linda Bowman, Chuanshu Huang, Stephen Leonard, Liying Wang, Val Vallyathan, Vince Castranova, and Xianglin Shi

From the Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505 and Nelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, New York 10987

Consumption of fruits and vegetables has been associated with a low incidence of cancers and other chronic diseases. Previous studies suggested that fresh apples inhibit tumor cell proliferation. Here we report that oral administration of apple peel extracts decreased the number of nonmalignant and malignant skin tumors per mouse induced by 12-O-tetradecanolyphorbol-13-acetate (TPA) in 7,12-dimethylbenz(a)anthracene-initiated mouse skin. ESR analysis indicated that apple extract strongly scavenged hydroxyl (OH) and superoxide () radicals. Mechanistic studies showed that pretreatment with apple peel extract inhibited AP-1 transactivation induced by ultraviolet B irradiation or TPA in JB6 cells and AP-1-luciferase reporter transgenic mice. This inhibitory effect appears to be mediated by the inhibition of ERKs and JNK activity. The results provide the first evidence that an extract from fresh apple peel extract may inhibit tumor promoter-induced carcinogenesis and associated cell signaling, and suggest that the chemopreventive effects of fresh apple may be through its antioxidant properties by blocking reactive oxygen species-mediated AP-1-MAPK activation.

Received for publication, October 20, 2003 , and in revised form, December 5, 2003.

^* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed. Tel.: 304-285-6229; Fax: 304-285-5938; E-mail: mid5{at}cdc.gov.

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