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Mechanisms and Biomarkers (WG 4) page 59
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were not univocal and promising (ATBC, 1994; Omenn et al.,1996; Hennekens et al., 1996).
Also the specific role of β-carotene in preventing DNA damage which is the base of cancer
development has been investigated, but mainly using supplements more than foods. Pool-
Zobel et al. (1997) found an effect of carrot juice intervention (330 ml, 22.3 mg β-carotene
and 15.7 mg α-carotene for 2 weeks) on endogenous and exogenous levels of strand breaks
in lymphocyte DNA and oxidative base damage.
The supplementation with 180 mg/week of β-carotene for 9 weeks was found to reduce the
frequency of micronucleated exfoliated cells from the buccal mucosa of tobacco and arecanut
chewers (Stich et al., 1984). The same effect was found for vitamin A but not
cantaxanthin suggesting that the inhibitory effect on the formation of micronuclei was due to
a mechanism not involving the scavenging of free radicals. Van Poppel et al. (1992) giving
20 mg/day β-carotene to heavy smokers found a reduction of micronuclei in sputum, and
hypothesized a role of β-carotene in preventing DNA damage in early stage of lung
carcinogenesis. It has been also reported (Umegaki et al., 1994) that the supplementation with
30 mg β-carotene for 13 days was able to protect human lymphocytes from x-ray induced
genetic damage (induction of micronuclei formation).
On the contrary the supplementation with 15 mg β-carotene twice daily for 6 weeks did not
affect mutagen sensitivity (Goodman et al., 1998) despite the 6 times increase in the
carotenoid plasma concentration. Other authors found no effect of β-carotene on oxidative
DNA damage in humans evaluated as 8-OHdG (van Poppel et al., 1995). Differently Lee et
al. (1998) reported a decrease of 8-OHdG in smokers after 9 mg β-carotene intake daily for 4
weeks even though the carotenoid was less effective with respect to vitamin E and C.
Vitamin C - Data in literature report that oxidative stress and smoking increase 8OHdG and
that reduced intake of ascorbate (5 mg/day) in males is correlated to higher sperm DNA
oxidation products that, on the contrary, are lowered after resupplementation with 60 mg/day
vitamin C (Fraga et al., 1996). As also reported by a recent review by Carr and Frei (1999a),
several studies showed an effect of vitamin C supplementation in the protection from DNA
oxidative damage (Pohl and Reidly, 1989; Green et al., 1994; Fraga et al., 1991; Lee et al,
1998; Panayotidis 1997; Brennan, 1996) however at doses that exceed those in tomato
products (60-1000 mg vitamin C). Other authors did not find any effect of vitamin C
supplementation both on in vivo or ex vivo DNA damage (Prieme et al., 1997; Anderson et
al., 1997) while in some cases there was a decrease or an increase depending on the marker