Journal Article

Dietary antioxidant depletion: enhancement of tumor apoptosis and inhibition of brain tumor growth in transgenic mice

Rudolf I. Salganik, Craig D. Albright, Jerilyn Rodgers, John Kim, Steven H. Zeisel, Mikhail S. Sivashinskiy and Terry A. Van Dyke

in Carcinogenesis

Volume 21, issue 5, pages 909-914
Published in print May 2000 | ISSN: 0143-3334
Published online May 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.5.909
Dietary antioxidant depletion: enhancement of tumor apoptosis and inhibition of brain tumor growth in transgenic mice

More Like This

Show all results sharing this subject:

  • Clinical Cytogenetics and Molecular Genetics

GO

Show Summary Details

Preview

Apoptosis, or regulated cell suicide, eliminates unwanted and damaged cells, including precancerous and cancerous cells. Since reactive oxygen species (ROS) act as essential apoptotic mediators, we reasoned that increasing the ROS level might enhance apoptosis and thereby slow down tumor growth. Here, using a defined transgenic brain tumor model with known tumor apoptosis rates, we test the impact of antioxidant-depleted diet, capable of increasing ROS levels, or antioxidant-enriched diets on tumor growth. Dramatically increased apoptosis occurs within tumors, but not in normal tissues of antioxidant-depleted mice. The presence of detectable increased oxidant stress within tumors indicates that the likely mechanism of enhanced tumor apoptosis is via ROS and DNA oxidative impairment. Importantly, due to the ROS-enhanced apoptosis, tumor growth is inhibited in mice fed an antioxidant-depleted diet. In clear contrast, an antioxidant-rich diet had no impact on tumor growth.

Keywords: CP, choroid plexus; LPV, lymphotopic papovavirus; 8-oxo-deoxyGua, 8-oxodeoxyguanine; 8-oxo-Gua, 8-oxo-guanine; ROS, reactive oxygen species.

Journal Article.  4606 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.