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Mechanisms and Biomarkers (WG 4) page 58
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(Meydani and Tengerdy, 1993; Harapanhalli et al., 1994). For this reason the effect of
vitamin E supplementation above normal dietary intake was tested with respect to genetic
damage rate in human lymphocytes (Fenech et al., 1997). Despite the increase in plasma
vitamin E concentration after the intake of 50 and 300 mg for 8 weeks, there was no apparent
relation between plasma vitamin E and endogenous or exogenous (exposure to hydrogen
peroxide) chromosome damage (micronuclei frequency) in healthy individuals. Also
Goodman et al. (1998) found the same results evaluating the bleomycin-induced
chromosomal damage after the supplementation with 400 IU α-tocopherol twice daily for 6
weeks. Higher doses (2 x 400 IU vitamin E for 6 weeks) did not reduce DNA damage
evaluated in Peripheral Blood Leukocytes treated with H2O2 (Brennan, 1996). Hartmann et
al. (1995) demonstrated that high doses of vitamin E (1200 mg /daily for 14 days) can
prevent exercise-induced DNA damage while high doses of a multivitamin mixture increased
the baseline level of DNA damage probably because of the large amount of trace metals also
present.
It has been reported that dietary modification can affect DNA oxidative damage in healthy
humans. For example the oxidation of cellular membranes (e.g. increased PUFA intake) has
been hypothesized as an important aspect of the mechanism for DNA damage, thus
compounds such as vitamin E that is a lipid peroxidation chain-breaking antioxidant in cell
membranes may provide protection.
Recently a crossover design consisting in a solid diet (5 days) followed by 10 days of
consumption of two different nutritionally complete liquid formula with low PUFA/high
vitamin E (ratio: 1.1) or high PUFA/low vitamin E (ratio: 3.5) was used to verify whether this
intervention could be related with a decrease in 8OHdG/dG. The results obtained were
similar for both the formulas however the diet modification involved a 22% decrease in the
ratio supporting the hypothesis that modest dietary changes can improve protection from
DNA damage (Chen et al., 1999).
Jenkinson et al. (1999) also reported that a 15% increase in dietary PUFA determined higher
endogenous and exogenous DNA damage that was reduced by adding 80 mg α-
tocopherol/day in the diet, supporting the hypothesis that vitamin E may protect from DNA
damage through the inhibition of membrane lipid peroxidation.
β-carotene - Several human intervention studies have been performed to investigate the
potential protective effect of this carotenoid against some type of cancer, however the results