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ACTA BIOLOGICA CRACOVIENSIA

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16 TH INTERNATIONAL SYMPOSIUM ON CAROTENOIDS<br />

Among other parameters we analyzed the formation of<br />

thymine dimers, as a measure of direct DNA damage, in hdF<br />

exposed to UVB-light in the presence and absence of the<br />

carotenoids mentioned above. In cells preincubated with DHIR<br />

and IR a significant decrease in formation of thymine dimers was<br />

found, whereas the treatment with luteine had no effect. In the<br />

alkaline Comet assay similar effects were determined for the aromatic<br />

carotenoids. In this assay also luteine showed some protection<br />

but less pronounced than DHIR and IR. Additionly, the<br />

formation of reactive oxygen species (ROS) and intracellular zinc<br />

release were determined. Both parameters were decreased in<br />

cells preincubated with DHIR in comparison to untreated cells or<br />

to those treated with luteine, which had no effect (Lutter et al.,<br />

2010). The data provide further evidence for the high antioxidative<br />

capacity of DHIR and confirm the hypothesis that DHIR is<br />

protective against UVB-induced damage. As expected from the<br />

structure DHIR acts as a multifunctional antioxidant with radical<br />

scavenging and UVB absorbing properties.<br />

REFERENCES<br />

MARTIN HDD, KOCK S, SCHERRERS R, LUTTER K, WAGENER T, HUNDSDÖRFER<br />

C, FRIXEL S, SCHAPER K, ERNST H, SCHRADER W, GÖRNER H,STAHL<br />

W. 2009. 3,3´-Dihydroxyisoreniera-tene, a natural carotenoid<br />

with superior antioxidant and photoprotective properties. Angew<br />

Chem Int Ed 48: 400-403.<br />

LUTTER K, DE SPIRT S, KOCK S, KRÖNKE KD, MARTIN HD, WAGENER T,<br />

STAHL W. 2010. 3,3´-Dihydroxyisorenieratene prevents UV-induced<br />

formation of reactive oxygen species and the release of proteinbound<br />

zinc ions in human skin fibroblasts. Mol Nutr Food Res<br />

54: 285-91.<br />

4.6.<br />

Beta-cryptoxanthin inhibits lung tumor by<br />

suppressing α7 nicotinic receptor expression<br />

and AKT activation in A/J mouse model<br />

Anita Iskandar, Chun Liu, Hansgeorg Ernst,<br />

Xiang-Dong Wang<br />

Human Nutrition Research Center on Aging, Tufts University,<br />

711 Washington St., Boston, MA, U.S.A., 02111,<br />

Anita.iskandar@tufts.edu, Chun.liu@tufts.edu,<br />

Xiang-dong.wang@tufts.edu<br />

The efficacy of beta-cryptoxanthin (BCX) for lung carcinogenesis<br />

has not been studied despite its association with a reduced risk<br />

of lung cancer in epidemiological studies. The activation of nicotinic<br />

acetylcholine receptor α7 subunit (α7-nAChR) and its downstream<br />

pathway can promote lung tumor growth. We hypothesize<br />

that BCX prevents the tobacco carcinogen-induced lung tumorigenesis<br />

by targeting α7-nAChR signaling. Male A/J mice were randomly<br />

assigned to six groups (n=16): the experimental arm<br />

received the NNK (4-[N-nitrosomethylamino]-l-[3-pyridyl]-lbutanone)<br />

injection with or without supplementation with BCX at<br />

two doses (0.2 and 2 mg/kg/day); and the control arm without<br />

NNK injection received the same BCX supplementation. The incidence<br />

and multiplicity of lung tumor and α7-nAChR expression<br />

and AKT activation were examined after 16 weeks post the carcinogen<br />

injection. There were 52% and 63% reductions of lung<br />

tumor multiplicity in mice supplemented with BCX at two doses,<br />

respectively (P

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