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Dietary
antioxidant depletion: enhancement of tumor apoptosis and inhibition of brain
tumor growth in transgenic mice
Salganik RI, Albright CD, Rodgers J, Kim J, Zeisel SH, Sivashinskiy
MS, Van Dyke TA
Department of Nutrition, School of Public Health, School
of Medicine, University of North Carolina, Chapel Hill, NC 27599, USA. rsalganik@unc.edu
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.
PMID: 10783311 [PubMed - indexed for
MEDLINE]
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