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antioxidants effect of coffee/which one has the hi'est antiox?
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antioxidants effect of coffee/which one has the hi'est antiox?

Effect of roasting on the antioxidant activity of coffee brews. del Castillo MD, Ames JM, Gordon MH. J Agric Food Chem. 2002 Jun 19;50(13):3698-703.
School of Food Biosciences, The University of Reading, Whiteknights, Reading, UK

Colombian Arabica coffee beans were roasted to give light, medium, and dark samples. Their aqueous extracts were analyzed by gel filtration chromatography, UV-visible spectrophotometry, capillary electrophoresis, and the ABTS(*)(+) assay. A progressive decrease in antioxidant activity (associated mainly with chlorogenic acids in the green beans) with degree of roasting was observed with the simultaneous generation of high (HMM) and low molecular mass (LMM) compounds possessing antioxidant activity. Maximum antioxidant activity was observed for the medium-roasted coffee; the dark coffee had a lower antioxidant activity despite the increase in color. Analysis of the gel filtration chromatography fractions showed that the LMM fraction made a greater contribution to total antioxidant activity than the HMM components.
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In vitro and ex vivo antihydroxyl radical activity of green and roasted coffee. Daglia M, Racchi M, Papetti A, et al. J Agric Food Chem. 2004 Mar 24;52(6):1700-4.
Department of Pharmaceutical Chemistry, Faculty of Pharmacy, University of Pavia, Pavia, Italy.

The specific antiradical activity against the hydroxyl radical of the water soluble components in green and dark roasted Coffea arabica and Coffea robusta coffee samples, both in vitro by the chemical deoxiribose assay and ex vivo in a biological cellular system (IMR32 cells), were determined. All the tested coffee solutions showed remarkable antiradical activity. In the deoxiribose assay, all the tested solutions showed similar inhibitory activity (IA%) against the sugar degradation (IA values ranged from 45.2 to 46.9%). In the cell cultures, the survival increase (SI%) ranged from 197.0 to 394.0% with C. robusta roasted coffee being significantly more active than the other samples. The coffee solutions underwent dialysis (3500 Da cutoff membrane) to fraction their components. In both systems, the dialysates (MW  3500 Da) from the roasted coffee samples were active. The preparative gel-filtration chromatography of roasted coffee C. robusta dialysate gave three fractions active in the biological system, all containing chlorogenic acid derivatives. The most active fraction was found to be that containing the 5-O-caffeoilquinic acid, which shows a linear relation dose-response ranging from 0.02 to 0.10 mM. The results show that both green and roasted coffee possess antiradical activity, that their more active component is 5-O-caffeoyl-quinic acid, and moreover that roasting process induces high MW components (later Maillard reaction products, i.e., melanoidins), also possessing antiradical activity in coffee. These results could explain the neuroprotective effects found for coffee consumption in recent epidemiological studies.
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Liver function

Overview
Two meta-analyses conclude that the available prospective cohort and case-control studies all show an inverse association between moderate coffee consumption and liver cancer, suggesting that an increased consumption of coffee may reduce the risk of liver cancer.
The results of the prospective cohort studies, in particular, are indicative of a dose-response relationship. Two extra cups of coffee per day are associated with a 43% reduced risk of liver cancer, amongst populations who typically consume anything from 1 to over 5 cups a day.
Several studies using patients have been published recently. They should be interpreted with caution, both because of possible flaws in their design and their small sample sizes.
One recent noteworthy study in patients with advanced hepatitis C-related liver disease suggests that regular, moderate coffee consumption is associated with lower rates of disease progression.
It is not yet clear whether, and to what extent, caffeine is implicated in the inverse association between coffee consumption and these liver diseases. Several possible mechanisms are under investigation:
The main primary caffeine metabolite, paraxanthine, appears to suppress the synthesis of CTGF (connective tissue growth factor) via a cascade of control cycles, which subsequently slows down the progression of liver fibrosis, cirrhosis and liver cancer.
Other alternative mechanisms are related to the anti-carcinogenic effects of cafestol and kahweol, and possible antiviral effects of chlorogenic acids and caffeic acid.
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MOLECULAR MECHANISMS OF CAFFEINE IN THE PREVENTION OF EXPERIMENTAL LIVER CIRRHOSIS
D. Gordillo-Bastidas1; E. Oceguera-Contreras1; A. M. Salazar Montes1; J. Gonzalez-Cuevas1; J. Armendáriz-Borunda1, 2
1. Molecular Biology and Genomics, Universidad de Guadalajara, Guadalajara Jalisco, Jalisco, Mexico.
2. OPD hospital civil de Guadalajara, Guadalajara , Mexico.

INTRODUCTION: Liver cirrhosis is determined by hepatic stellate cells activation, and is perpetuated by growth factors and pro-inflammatory molecules. It has been observed that caffeine (CFA) modifies these signaling pathways in vitro, but there are no in vivo studies demonstrating this effect.
AIM: to determine the molecular mechanisms by which CFA prevents experimental liver cirrhosis. METHODS: Liver cirrhosis was induced in Wistar rats by chronic intoxication with thioacetamide (TAA) and bile duct ligation (BDL). Animals were treated daily with CFA (15mg/kg) via orogastric. Rats were sacrificed, liver biopsies and blood was obtained. We evaluated the fibrosis degree in histological sections stained with Masson, inflammatory infiltrate with hematoxylin and eosin, and immunohistochemistry for CD11b. We analyzed gene expression by QRT-PCR for Col-1, CTGF, TGF-b1, TNF-a, IL-1b, IL-6, SOD and CAT. We performed an enzyme activity assay for CAT and SOD. RESULTS: Groups that received CFA showed fewer inflammatory infiltrate as verified by immunohistochemistry for CD11b. Percentage of fibrosis was reduced in 80% (p <0.0001) in TAA+CFA group, and 38% (p <0.0001) in BDL+CFA group. Expression of CTGF, Col-1 and TGFβ1 was lower in 3.5 (p <0.01), 3.5 (p <0.05) and 3 (p <0.01) fold in TAA+CFA, and was lower at 5.0 (p <0.01) fold for CTGF and 3.0 (p <0.01) fold for Col-1 in BDL+CFA group. Expression of TNF-α, IL-6 and IL-1β was lower by 1.6 (p <0.06) 6.0 (p <0.05) and 9 (p <0.01) fold in TAA+CFA, 9.4 (p <0.001) for TNF-a and 5.0 (p <0.001) fold for IL-6 in BDL+CFA group. Expression of SOD and CAT was greater in 1.5 (p <0.05) and 9 (p <0.05) fold in TAA+CFA, and 1.6 (p <0.05) and 211 (p <0.05) fold in BDL+CFA. CAT zymography showed increased biological activity in the BDL+CFA group (p <0.0001). CONCLUSIONS: CFA has a powerful effect to limit profibrogenic and proinflammatory response despite the presence of an inducer of liver damage. Mechanisms by which CFA prevents liver cirrhosis are, lowering of expression of growth factors and proinflammatory cytokines, and increased activity and expression of antioxidant enzymes.
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