Antioxidant effectiveness of coffee extracts and selected constituents in cell-free systems and human colon cell lines.
METHODS
Epidemiological studies suggest that coffee can reduce the risk of degenerative diseases such as diabetes type 2, cardiovascular disease and cancer. These beneficial effects have partly been attributed to the antioxidant activity of coffee. We determined composition and antioxidant potential of differentially roasted coffee extracts and investigated the impact of selected original constituents and roast products.


RESULTS
Parameters studied were direct antioxidant activity (trolox equivalent antioxidant capacity/oxygen radical absorbing capacity), cellular reactive oxygen species (ROS) level, DNA damage and protein expression of NAD(P)H: quinone oxidoreductase, γ-glutamylcysteine ligase and glutathione reductase in HT-29/Caco-2 cells at 24-h incubation. All extracts showed distinct direct antioxidant activity: medium roasts>light roast AB1 (caffeoylquinic acid (CQA)-rich Arabica Brazil extract); dark roast AB2 (N-methylpyridinium (NMP)-rich Arabica Brazil extract), and diminished t-butylhydroperoxide-induced ROS level in HT-29 cells (AB2>medium roasts>AB1). NAD(P)H:quinone oxidoreductase 1 expression and γ-glutamylcysteine ligase expression were distinctly induced by AB1 and 5-CQA, but not by AB2 and NMP. 5-CQA and caffeic acid exhibited highest trolox equivalent antioxidant capacity/oxygen radical absorbing capacity values (5-CQA: 1.3/3.5 mM and caffeic acid: 1.3/3.9 mM trolox); ROS level was distinctly diminished by 5-CQA (≥3 μM), catechol (30 μM) and trigonelline (≥30 μM), whereas menadione-induced DNA damage in Caco-2 cells was reduced by NMP compounds (1-30 μM).


CONCLUSIONS
The results emphasize that both original constituents and roast products contribute to the cellular antioxidant effectiveness of coffee.
Bakuradze
Tamara
T
Department of Chemistry, Division of Food Chemistry and Toxicology, University of Kaiserslautern, Kaiserslautern, Germany.
Lang
Roman
R
Hofmann
Thomas
T
Stiebitz
Herbert
H
Bytof
Gerhard
G
Lantz
Ingo
I
Baum
Matthias
M
Eisenbrand
Gerhard
G
Janzowski
Christine
C
D000975:Antioxidants / Q000494:pharmacology*; D018938:Caco-2 Cells; D002109:Caffeic Acids / Q000494:pharmacology; D002474:Cell-Free System / Q000378:metabolism; D003069:Coffee / Q000737:chemistry*; D003106:Colon / Q000166:cytology* / Q000378:metabolism*; D004249:DNA Damage; D005721:Glutamate-Cysteine Ligase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D019073:HT29 Cells; D006801:Humans; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000378:metabolism; D010936:Plant Extracts / Q000494:pharmacology*; D011726:Pyridinium Compounds / Q000494:pharmacology; D011801:Quinic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000032:analysis; D020122:tert-Butylhydroperoxide / Q000494:pharmacology
D000975:Antioxidants; D002109:Caffeic Acids; D003069:Coffee; D010936:Plant Extracts; D011726:Pyridinium Compounds; D017382:Reactive Oxygen Species; C472707:caffeoylquinic acid; D011801:Quinic Acid; C014677:1-methylpyridinium; D020122:tert-Butylhydroperoxide; D016660:NAD(P)H Dehydrogenase (Quinone); D005980:Glutathione Reductase; D005721:Glutamate-Cysteine Ligase; C040048:caffeic acid