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Effect of coffee Melanoidin on human hepatoma HepG2 cells. Protection against oxidative stress induced by tert ‐butylhydroperoxide
Author(s) -
Goya Luis,
DelgadoAndrade Cristina,
RufiánHenares José A.,
Bravo Laura,
Morales Francisco J.
Publication year - 2007
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200600228
Subject(s) - oxidative stress , melanoidin , chemistry , glutathione , lactate dehydrogenase , reactive oxygen species , antioxidant , malondialdehyde , glutathione reductase , glutathione peroxidase , biochemistry , viability assay , glutathione disulfide , microbiology and biotechnology , cell , enzyme , superoxide dismutase , biology , maillard reaction
Soluble high‐molecular weight fraction (named melanoidin) from coffee brew was isolated by ultrafiltration, subsequently digested by simulating a gastric plus pancreatic digestive condition and partly characterized by CZE, gel‐filtration and browning. The objective of the present study was to investigate the potential protective effect of the coffee melanoidin submitted to gastrointestinal digestion on cell viability (lactate dehydrogenase leakage) and redox status of cultured human hepatoma HepG2 cells submitted to oxidative stress induced by tert ‐butylhydroperoxide ( t ‐BOOH). Concentration of reduced glutathione (GSH) and malondialdehyde (MDA), generation of reactive oxygen species (ROS) and activity of antioxidant enzymes glutathione peroxidase (GPx) and reductase (GR) were used as markers of cellular oxidative status. Pretreatment of cultured HepG2 cells with 0.5–10 μg/mL digested coffee melanoidin (DCM) for 2 or 20 h completely prevented the increase in cell damage and GR and partly prevented the decrease of GSH and the increase of MDA and GPx evoked by t ‐BOOH in HepG2 cells. In contrast, increased ROS generation induced by t ‐BOOH was not prevented when cells were pretreated with DCM. The results show that treatment of HepG2 cells with concentrations of DCM within the expected physiological range confers the cells a significant protection against an oxidative insult.