2019
n-3 Polyunsaturated fatty acids alter benzo[a]pyrene metabolism and genotoxicity in human colon epithelial cell models
TYLICHOVÁ, Zuzana; Jiri NECA; Jan TOPINKA; Alena MILCOVA; Jiřina HOFMANOVÁ et al.Základní údaje
Originální název
n-3 Polyunsaturated fatty acids alter benzo[a]pyrene metabolism and genotoxicity in human colon epithelial cell models
Autoři
TYLICHOVÁ, Zuzana; Jiri NECA; Jan TOPINKA; Alena MILCOVA; Jiřina HOFMANOVÁ; Alois KOZUBÍK; Miroslav MACHALA a Jan VONDRÁČEK
Vydání
Food and Chemical Toxicology, OXFORD, PERGAMON-ELSEVIER SCIENCE LTD, 2019, 0278-6915
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30304 Public and environmental health
Stát vydavatele
Velká Británie a Severní Irsko
Utajení
není předmětem státního či obchodního tajemství
Odkazy
Impakt faktor
Impact factor: 4.679
Označené pro přenos do RIV
Ano
Kód RIV
RIV/00216224:14310/19:00113499
Organizační jednotka
Přírodovědecká fakulta
UT WoS
EID Scopus
Klíčová slova anglicky
Colon cancer; Eicosapentaenoic acid; Docosahexaenoic acid; Polycyclic aromatic hydrocarbon; DNA damage
Štítky
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 16. 4. 2020 14:51, Mgr. Michal Petr
Anotace
V originále
Dietary carcinogens, such as benzo[a]pyrene (BaP), are suspected to contribute to colorectal cancer development. n-3 Polyunsaturated fatty acids (PUFAs) decrease colorectal cancer risk in individuals consuming diets rich in PUFAs. Here, we investigated the impact of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acid on metabolism and genotoxicity of BaP in human cell models derived from the colon: HT-29 and HCT-116 cell lines. Both PUFAs reduced levels of excreted BaP metabolites, in particular BaP-tetrols and hydroxylated BaP metabolites, as well as formation of DNA adducts in HT-29 and HCT-116 cells. However, EPA appeared to be a more potent inhibitor of formation of some intracellular BaP metabolites, including BaP-7,8-dihydrodiol. EPA also reduced phosphorylation of histone H2AX (Ser139) in HT-29 cells, which indicated that it may reduce further forms of DNA damage, including DNA double strand breaks. Both PUFAs inhibited induction of CYP1 activity in colon cells determined as 7-ethoxyresorufin-O-deethylase (EROD); this was at least partly linked with inhibition of induction of CYP1A1, 1A2 and 1B1 mRNAs. The downregulation and/or inhibition of CYP1 enzymes by PUFAs could thus alter metabolism and reduce genotoxicity of BaP in human colon cells, which might contribute to known chemopreventive effects of PUFAs in colon epithelium.