Investigation of genotoxic properties of green tea extract (CROSBI ID 547931)
Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | međunarodna recenzija
Podaci o odgovornosti
Durgo, Ksenija ; Kostić, Sandra ; Kopjar, Nevenka, Osmak, Maja ; Franekić Čolić, Jasna
engleski
Investigation of genotoxic properties of green tea extract
Green tea, widely consumed beverage, is produced from the plant Camellia sinensis and contains flavonoids that are considered to play an important role in cancer prevention. The most important mechanisms of their function are scavenging free radicals and suppressing ROS (reactive oxygen species) formation. The aim of this study was to evaluate potential genotoxic effect of green tea extract (obtained after 5 min of loose leaves extraction with 10% ethanol solution), epigallocatechin gallate (EGCG) and epicatechin gallate (ECG) on human laryngeal carcinoma cell line (HEp2) and their resistant subline (CK2). EGCG and ECG are most abundant compounds in green tea extract. In such purpose cytotoxic effects of different concentrations of green tea, EGCG and ECG in different time of exposure were determined. Also, we have measured their ability to induce lipid peroxidation (TBA-MDA formation) and primary damage of DNA (comet assay). The results of this study demonstrate that EGCG and green tea extract induced increased genotoxicity of resistant CK2 cell line after shorter incubation time. Investigated compounds showed higher degree of cytotoxicity in longer period of incubation. Green tea extract induces lipid peroxidation in CK2 cell line. Investigated catechins reduce basal primary DNA damage in HEp2 cells, whereas green tea extract, after prolonged incubation, induces single and double strand breaks. Investigated compounds do not induce any damage in CK2 cell line. Genotoxic effects strongly depend on green tea concentration and on incubation time.
citotoxicity; comet assay; ECG; EGCG; green tea
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
Podaci o prilogu
S101-S101.
2008.
objavljeno
Podaci o matičnoj publikaciji
Dekant, W.
Elsevier