2011 Cilt 5 Sayı 14

Permanent URI for this collectionhttps://hdl.handle.net/11452/16912

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Browsing by Subject "Aflatoxin b1"

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    Dermatocarpon intestiniforme (a lichen) modulates aflatoxin B1 induced genetic and oxidative damage in vitro
    (Uludağ Üniversitesi, 2011) Turkez, Hasan; Dirican, Ebubekir; Aydin, Elanur; Togar, Basak; Celik, Kubra
    Aflatoxin B1 (AFB1), a worldwide toxic contaminant of foods produced by Aspergillus species, exhibits oxidative stress mediated genotoxic damage although, the mechanism of cellular damage caused by AFB1 has not been fully elucidated. Different antioxidant molecules such as ascorbic acid, beta-carotene and tocopherol have been shown to possess anti-carcinogenic and anti-mutagenic properties against AFB1 toxicity. On the other hand, lichens have long been investigated popularly for biological roles; mainly anti-tumor, anti-microbial and anti-oxidant activities. Also, the influence of lichenic substances on DNA binding of AFB1, in mammalian cells, is still unknown. Therefore, in this study, we aimed to determine whether Dermatocarpon intestiniforme extracts conferred a protection against AFB1-induced genotoxic and oxidative damage in vitro. For this aim, we determined sister chromatid exchange (SCE) rates and main antioxidant enzyme activities including superoxide dismutase (SOD) and catalase (CAT) in AFB1 (10 µM) and lichen (1, 5, 10, 25, 50 and 100 µM) treated human whole blood cultures (n=3) for 72h. The lichen extracts at tested concentrations did not exhibit any negative effects on above studied parameters in culture tubes. Moreover, the results of the present study indicated that the increases of SCE frequencies and the decreases of antioxidant enzyme activities by AFB1 were minimized by the application of the lichen extracts (at 25 and 50 µM). Our results firstly suggest that D. intestiniforme augments the antioxidants defense against AFB1 induced toxicity. Again, these results demonstrate that dose controlled D. intestiniforme lichen diet may play a protective role in the process of AFB1 mutagenesis and/or carcinogenesis.