Open AccessDietary antioxidant depletion: enhancement of tumor apoptosis and inhibition of brain tumor growth in transgenic mice
Author(s) -
R. I. Salganik,
Craig D. Albright,
Jerilyn Rodgers,
John Kim,
Steven H. Zeisel,
Mikhail S. Sivashinskiy,
Terry A. Van Dyke
Publication year - 2000
Publication title -
carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.688
H-Index - 204
eISSN - 1460-2180
pISSN - 0143-3334
DOI - 10.1093/carcin/21.5.909
Subject(s) - apoptosis , reactive oxygen species , oxidative stress , antioxidant , genetically modified mouse , dna damage , programmed cell death , biology , transgene , microbiology and biotechnology , cancer research , chemistry , biochemistry , dna , gene
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.