Zinc is an essential trace mineral in humans, second only to iron in its abundance. Zinc plays an important role as a metal co-factor in a number of metalloproteins, some of which are enzymes. Within these proteins, zinc can function as a catalyst or as part of the structure of the protein itself. Zinc is needed for DNA binding proteins, reproduction, immunity and free radical defence. Estimates suggest that Worldwide, ≈2 billion people are deficient in zinc and large numbers of the World’s population are zinc insufficient. It was estimated in the National Health and Nutrition Examination Survey (NHANES) that ≥12% of Americans are deficient in zinc. Zinc status is difficult to measure because marginal deficiency does not show up in plasma or hair samples. Evidence suggests that zinc deficiency increases cancer risk, possibly because of its role as an antioxidant and in DNA damage repair.
Researchers1 have investigated the effects of zinc depletion and repletion on DNA strand breaks, antioxidant defences and oxidative stress. The subjects were nine healthy men aged between 19 and 50 years with reported zinc intakes ≥11 mg/d and with plasma zinc concentrations ≥74 µg/dL. Subjects were fed adequate zinc for 13 days, and then depleted of zinc (0.6 mg/d for 7d followed by 4mg /d; phytate was added to the diet to inhibit zinc absorption) up to day 55. From days 56 to 83 the subjects consumed 11 mg zinc with 20 mg/d of zinc as zinc gluconate for the first 7 days. The period of dietary zinc depletion was associated with increased DNA strand breaks in peripheral blood cells, and this effect was ameliorated during the period of zinc repletion. Zinc plasma levels showed a negative correlation with DNA strand breaks.
Zinc concentrations were 13% higher at the end of the repletion phase compared to the depletion phase, but interestingly zinc urine concentrations did not change significantly throughout the trial, highlighting the difficulty is measuring subtle changes in zinc status. Plasma antioxidant levels as measured by a FRAP assay did not change throughout the study, but α-tocopherol and γ-tocopherol plasma concentrations tended to rise during zinc depletion. Erythrocyte levels of the important antioxidant enzyme CuZnSOD (superoxide dismutase) showed a trend to decrease during zinc depletion and increase during zinc repletion. However these changes of CuZnSOD were not statistically significant. There was also no change in the levels of F2-isoprostanes from non-enzymatic peroxidation of arachidonic acid. These results suggest that zinc depletion increases DBA strand breaks, but does not cause significant changes to antioxidant defence in the short-term.
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