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Abstract
A large body of evidence suggests that a significant percentage of deaths resulting
from cancer in the United States could be avoided through greater attention to proper
and adequate nutrition. Although many dietary compounds have been suggested to contribute
to the prevention of cancer, there is strong evidence to support the fact that zinc,
a key constituent or cofactor of over 300 mammalian proteins, may be of particular
importance in host defense against the initiation and progression of cancer. Remarkably,
10% of the U.S. population consumes less than half the recommended dietary allowance
for zinc and are at increased risk for zinc deficiency. Zinc is known to be an essential
component of DNA-binding proteins with zinc fingers, as well as copper/zinc superoxide
dismutase and several proteins involved in DNA repair. Thus, zinc plays an important
role in transcription factor function, antioxidant defense and DNA repair. Dietary
deficiencies in zinc can contribute to single- and double-strand DNA breaks and oxidative
modifications to DNA that increase risk for cancer development. This review will focus
on potential mechanisms by which zinc deficiency impairs host protective mechanisms
designed to protect against DNA damage, enhances susceptibility to DNA-damaging agents
and ultimately increases risk for cancer.